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PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Curcumin, a natural polyphenol, has been reported to modulate various oncogenic signaling pathways, but its role in inhibiting IFN-γ-driven PD-L1 expression in NSCLC remains unclear.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
The NSCLC cell line A549 were treated with curcumin (50 µM) for 2 h before stimulation with IFN-γ (500 U/ml).
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Western blot, qRT-PCR, and immunofluorescence microscopy were used to evaluate STAT1 phosphorylation, PD-L1 expression, and the localization of phosphorylated STAT1 (p-STAT1).
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
The expression of interferon-stimulated genes (ISGs), including SOCS1 and ISG15, was also examined.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Additionally, the Resazurin assay was performed to assess cell viability.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
IFN-γ significantly induced STAT1 phosphorylation, leading to a time-dependent upregulation of PD-L1 expression.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Immunofluorescence confirmed that p-STAT1 is translocated to nucleus.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Curcumin treatment inhibited STAT1 phosphorylation by 68% (p < 0.001), leading to a marked reduction in PD-L1 expression.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Moreover, curcumin suppressed IFN-γ-induced SOCS1 (63%) and ISG15 (54%) expressions, indicating a broader effect on STAT1-mediated immune evasion.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Finally, curcumin enhanced IFN-γ-mediated growth inhibition, reducing cell viability by 47% at 48 h (p < 0.01).
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Curcumin effectively inhibits IFN-γ-induced STAT1 phosphorylation and PD-L1 expression, downregulates ISGs, and enhances IFN-γ-mediated tumor suppression.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
These findings suggest that curcumin may serve as a therapeutic adjuvant in NSCLC, potentially improving immune checkpoint inhibitor (ICI) efficacy.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Lung cancer continues to be the most prevalent cancer-related mortality globally, responsible for more than 1.8 million deaths per year (Siegel et al. 2024).
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Non-small cell lung cancer (NSCLC) accounts for ~ 85% of all lung cancer cases, an issue that is of significant public health importance and also a target for oncological research (Salih et al. 2025).
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Over the last decade, the development of immune checkpoint inhibitors (ICIs) targeting the programmed death- 1/programmed death-ligand 1 (PD- 1/PD-L1) axis has shifted the treatment landscape for NSCLC, significantly improving survival rates in a particular group of patients (Rizvi et al. 2015).
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Nevertheless, with these advancements, a large proportion of NSCLC patients either show a lack of responsiveness to ICIs (primary resistance) or develop resistance ("acquired resistance") over time that significantly restricts their clinical efficacy (Sharma et al. 2017; Rotte 2019).
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Immune evasion of NSCLC is significantly attributed to the expression of PD-L1, a transmembrane molecule that binds to PD- 1 receptors located on cytotoxic T cells and induces immune suppression and tumor tolerance.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
PD-L1 overexpression is often linked to poor prognosis, tumor aggression, and poor response to ICIs (Rizvi et al. 2015; Kim and Chen 2016).
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
One of the major regulators of PD-L1 expression in the tumor microenvironment is IFN-γ, a key cytokine modulating the immune system.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Although IFN-γ is classically described to have tumor-suppressive effects, paradoxically, it also plays a pro-tumorigenic role by inducing PD-L1 expression, enabling tumor cells to escape immune surveillance (Garcia-Diaz et al. 2017).
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
IFN-γ signaling is largely achieved via Janus Kinase—Signal Transducer and Activator of Transcription (JAK-STAT) pathway and, in particular, via STAT1.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Binding of IFN-γ to its receptors, JAK1 and JAK2, phosphorylates STAT1 on Tyr701.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Upon phosphorylation, STAT1 dimerizes, translocate to the nucleus, and binds to gamma-activated sequence (GAS) motifs of the PD-L1 promoter, in turn increasing the level of PD-L1 transcription (Sumitomo et al. 2022).
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
As confirmed by several studies, IFN-γ-induced activation of STAT1 is one of the most potent inducers of PD-L1 expression in NSCLC, which in turn leads to adaptive immune resistance that prevents T-cell-mediated tumor destruction (Drake et al. 2006; Shin et al. 2017).
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Since IFN-γ levels are typically increased in the tumor microenvironment of NSCLC, strategies that can inhibit IFN-γ-driven upregulation of PD-L1 promise to be valuable for improving the efficacy of ICIs (Spranger et al. 2013).
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Despite extensive research regarding PD-L1 regulation in NSCLC, therapeutic approaches that specifically aim to silence IFN-γ-induced PD-L1 expression are still limited.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Strategies presently are based on ICIs in synergy with kinase inhibitors, epigenetic modulators, or chemotherapy, but such pharmacologic efforts are typically associated with toxicity and short-term failure (Zhou and Yang 2023).
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Accordingly, the discovery of non-toxic, naturally derived compounds that effectively and specifically suppress IFN-γ-mediated PD-L1 expression but do not negatively affect the host immune function is of significant interest.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Curcumin, a polyphenolic compound isolated from the extract of Curcuma longa (turmeric), has attracted attention as a multi-targeted therapeutic agent due to its anti-inflammatory, antioxidant, and anti-cancer functions (Allegra et al. 2017).
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
It has been shown to suppress a variety of oncogenic signaling pathways such as nuclear factor-kappa B (NF-κB), cyclooxygenase- 2 (COX- 2), STAT3, and AKT, leading to growth inhibition and apoptosis in a variety of cancers (Kumar et al. 2021).
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Several preclinical studies have suggested that curcumin can downregulate PD-L1 expression in different cancer models, including breast and colon cancer, by inhibiting STAT1 phosphorylation and preventing its nuclear translocation (Midura-Kiela et al. 2012).
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Nevertheless, its specific involvement in downregulating IFN-γ-induced PD-L1 expression in NSCLC, especially in A549 cells, is unknown.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
As high PD-L1 expression is associated with poor response to ICIs, understanding natural products (like curcumin) that could regulate IFN-γ-induced PD-L1 expression might provide new strategies for upgrading the outcome of NSCLC treatment.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Although these encouraging results are promising, there are some deficiencies in our knowledge about how curcumin functions in regulating IFN-γ/STAT1 signaling in lung cancer.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Firstly, while previous reports have shown that curcumin can block the phosphorylation of STAT1, they have not specifically evaluated the effect of curcumin on the expression of PD-L1 in NSCLC.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Second, the underlying mechanism of curcumin's inhibitory action on STAT1 is still unknown, especially whether curcumin directly inhibits STAT1 phosphorylation or inhibits its nuclear translocation.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Third, the ability of curcumin to enhance the efficacy of ICIs by decreasing PD-L1 expression has not been extensively studied, and this should be explored.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Given these gaps in knowledge, the present study aims to investigate the effect of IFN-γ on STAT1 phosphorylation and PD-L1 expression in A549 cells and determine whether curcumin can inhibit IFN-γ-induced STAT1 activation and subsequent PD-L1 upregulation.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
In addition, explore the impact of curcumin on IFN-γ-induced expression of interferon-stimulated genes (ISGs), such as SOCS1 and ISG15, which are involved in immune signaling and tumor immune escape, and evaluate whether curcumin enhances the anti-proliferative effects of IFN-γ, suggesting a potential therapeutic benefit beyond immune modulation.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Human non-small cell lung cancer (NSCLC) cell, A549, was obtained from American Type Culture Collection (ATCC) and cultured in Dulbecco's Modified Eagle Medium (DMEM) containing 10% fetal bovine serum (FBS) (Life Technologies), 1% penicillin–streptomycin, and 2 mM L-glutamine.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Cells were cultured in a humidified incubator at 37 °C and 5% CO₂ with regular 2–3-day passaging in a 0.25% trypsin–EDTA suspension.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
All experiments were performed on cells between passage 5 and passage 15, thereby permitting reproducibility.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Recombinant human IFN-γ was purchased from PeproTech (EC Ltd PeproTech, London, UK) and stored in sterile phosphate-buffered saline (PBS) at 10 U/ml stock concentration.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Curcumin ≥ 95% was purchased from Santa Cruz (Heidelberg, Germany) and dissolved in dimethyl sulfoxide (DMSO) (≥ 99.9% purity) to make a 50-mM solution.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
The working dilutions of curcumin were freshly prepared in the complete DMEM prior to each experiment.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Cells were pretreated with curcumin (50 µM) for 2 h prior to the IFN-γ (500 U/ml) stimulation for studied time points.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Control groups were treated with vehicle (DMSO < 0.1%).
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Cell viability was assessed using the Resazurin assay (Sigma-Aldrich, #R7017 - 1G).
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
A549 cells were seeded in 96-well plates at a density of 3 × 10 cells per well (final volume of 100 μL/well) and allowed to adhere overnight.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Following 24 h treatment with IFN-γ, curcumin, or a combination of both, 20 µl of Resazurin reagent (0.15 mg/ml) was then added to each well, and incubation was performed for 2–4 h at 37 °C.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
The conversion of Resazurin to resorufin was measured by fluorescence using a microplate reader (excitation 560 nm, emission 590 nm) or by absorbance at 570 nm with 600 nm as a reference wavelength.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Cell viability was determined as a percentage compared to untreated control cells.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Cell Viability (%) = (Absorbance of control cells of treated cells​) × 100.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Total protein lysates were extracted from treated A549 cells using ice-cold radioimmunoprecipitation assay (RIPA) buffer supplemented with protease and phosphatase inhibitors and centrifuged at 10,000 × g for 10 min at 4◦C. The total protein concentrations were measured with the bicinchoninic acid (BCA) protein assay kit (Pierce, Thermo Fisher Scientific, USA).
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Equal amounts of protein (20 μg per sample) were separated on 10% sodium dodecyl sulfate–polyacrylamide gels (SDS-PAGE) and transferred onto 0.45 μM nitrocellulose membranes (Merck).
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Membranes were blocked with 5% BSA in Tris-buffered saline with 0.1% Tween- 20 (TBST) for 1 h at room temperature to prevent non-specific binding and incubated overnight at 4 °C with primary antibodies against phospho-STAT1 (Tyr701), total STAT1, PD-L1, and β-actin (Santa Cruz Biotechnology, Dallas, TX, USA).
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
After washing with TBST, membranes were incubated with horseradish peroxidase (HRP)-conjugated secondary anti-mouse IgG antibody or anti-rabbit IgG, HRP-linked antibody, for 1 h at room temperature.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Protein bands were detected using enhanced chemiluminescence (ECL) reagent (GE Healthcare, USA) and visualized using a ChemiDoc imaging system (Bio-Rad, USA).
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Analysis of protein bands was performed using ImageJ software (NIH, Bethesda, MD, USA).
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
The primary and secondary antibodies are listed in Table 1.Table 1The description of primary and secondary antibodiesAntibodySpeciesCloneDilutionCa#SourcePD-L1RabbitMonoclonal1:1000ab213524AbcamSTAT1MouseMonoclonal1:10009176Cell Signaling TechnologypSTAT1RabbitMonoclonal1:10009177SCell Signaling Technologyβ-actinMouseMonoclonal1:500047,778Santa Cruz Biotechnology, Dallas, TX, USAAnti-mouseHorse-1:10,0007076Cell Signaling, Danvers, MA, USAAnti-RabbitGoat-1:10,0007074Cell Signaling, Danvers, MA, USA The description of primary and secondary antibodies Total RNA was extracted from A549 cells using the RNeasy Mini-Kit (Qiagen, #74,104) according to the manufacturer’s instructions, and the eluted RNA purity and concentration were assessed using a NanoDrop One spectrophotometer (Thermo Scientific, USA).
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
For cDNA synthesis, 500 ng of RNA was reverse transcribed using the RevertAid First Strand cDNA Synthesis Kit to cDNA as per the manufacturer’s instructions.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Quantitative real-time PCR (qRT-PCR) was conducted using the SYBR Green PCR Master Mix (Applied Biosystems™) on a QuantStudio 5 Machine (Thermo Fisher Scientific, Inc.).
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
The relative expression levels of PD-L1, STAT1, and ISGs (ISG15 and SOCS1) were normalized to the housekeeping gene GAPDH and analyzed using the 2^ − ΔΔCt method.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
The PCR reactions were carried out in duplicate with 40 cycles of denaturation (15 s at 95 °C), annealing (20 s at 65 °C), and elongation (20 s at 72 °C) after an initial enzyme activation (15 min at 95 °C).
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
The primer sequences used are presented in Table 2.Table 2List of PCR primers designed using NCBI/Primer-BLAST programPrimerPrimer sequencesForwardReverseCD274 ()5′-TGGCATTTGCTGAACGCATTT- 3′5′-AGTGCAGCCAGGTCTAATTGT- 3′ISG155′-ATCACCCAGAAGATCGGCGT- 3′5′-TCGCATTTGTCCACCACCAG- 3′SOCS15’- TTCGCCCTTAGCGTGAAGATGG- 3′5’- TAGTGCTCCAGCAGCTCGAAGA- 3′GAPDH5′-GGAAGGTGAAGGTCGGAGTC- 3′5′-TGAAGGGGTCATTGATGGCA- 3′ List of PCR primers designed using NCBI/Primer-BLAST program A549 cells were seeded onto sterile coverslips in 12-well plates and treated as described.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
After incubation, cells were fixed with 4% paraformaldehyde for 15 min and permeabilized with 0.1% Triton X- 100 for 10 min.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
After blocking with 1% bovine serum albumin (BSA) for 30 min, cells were incubated overnight at 4 °C with primary antibodies against PD-L1 and phospho-STAT1.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Following PBS washes, cells were incubated with Alexa Fluor 488- or 594-conjugated secondary antibodies for 1 h at room temperature.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Nuclei were counterstained with DAPI, and images were captured using a fluorescence microscope (Zeiss Axio Observer, Germany).
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
All experiments were performed in triplicate, and data are presented as mean ± standard deviation (SD).
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Statistical analyses were conducted using GraphPad Prism 10 (GraphPad Software, USA).
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
One-way analysis of variance (ANOVA) followed by Tukey’s post-hoc test was used to compare multiple groups, and an unpaired Student’s t-test was used for pairwise comparisons.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Differences were considered statistically significant at p < 0.05.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
STAT1 phosphorylation at tyrosine 701 (Tyr701) is a key regulatory event in IFN-γ-mediated signaling, leading to STAT1 dimerization, nuclear translocation, and transcriptional activation of ISGs, including PD-L1.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
To confirm the activation of the JAK-STAT1 pathway in A549 cells, we analyzed phospho-STAT1 (Tyr701) levels by Western blotting after stimulation with 500 U/ml of IFN-γ for different time points (0, 1, 2, 6, 12, and 24 h).
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Our results demonstrated a time-dependent increase in STAT1 phosphorylation.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
A significant induction observed as early as 30 min post-treatment (p < 0.01), peaking at 2 h (p < 0.001), and remaining elevated up to 24 h. Total STAT1 protein levels remained unchanged across all time points, indicating that the increase in phospho-STAT1 was due to phosphorylation rather than upregulation of STAT1 expression, as shown in Fig. 1.Fig.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
1Western blot analysis showing STAT1 phosphorylation and PD-L1 expression in A549 NSCLC cells following IFN-γ treatment.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
A549 cells were treated with 500 U/mL of IFN-γ for various time points (0, 30 min, 1 h, 2 h, and 24 h).
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Protein lysates were collected and analyzed by Western blot using antibodies against phosphorylated STAT1 (Tyr701), total STAT1, and PD-L1.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
β-Actin was used as a loading control Western blot analysis showing STAT1 phosphorylation and PD-L1 expression in A549 NSCLC cells following IFN-γ treatment.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
A549 cells were treated with 500 U/mL of IFN-γ for various time points (0, 30 min, 1 h, 2 h, and 24 h).
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Protein lysates were collected and analyzed by Western blot using antibodies against phosphorylated STAT1 (Tyr701), total STAT1, and PD-L1.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
β-Actin was used as a loading control To further investigate the effect of IFN-γ on STAT1 activation, we performed immunofluorescence microscopy to visualize the cellular localization of phosphorylated STAT1 (p-STAT1) in A549 cells following a 2-h treatment with IFN-γ (500 U/ml).
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
In untreated control cells, STAT1 was primarily localized in the cytoplasm, with minimal nuclear fluorescence detected.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
However, upon IFN-γ stimulation, a marked increase in nuclear accumulation of p-STAT1 was observed, as shown in Fig. 2, indicating its activation and translocation to the nucleus, where it functions as a transcription factor.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
This translocation pattern was confirmed through co-staining with DAPI, a nuclear marker, which showed strong co-localization of p-STAT1 within the nucleus.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Fig. 2Immunofluorescence microscopy showing p-STAT1 localization in A549 cells treated with IFN-γ.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
A549 cells were treated with 500 U/mL of IFN-γ for 2 h, then analyzed by immunofluorescence microscopy to assess p-STAT1 localization.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
In untreated cells, p-STAT1 was primarily detected in the cytoplasm.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Following IFN-γ treatment, increased nuclear localization of p-STAT1 was observed.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
DAPI was used for nuclear staining, and β-actin staining was used to visualize the cytoskeleton Immunofluorescence microscopy showing p-STAT1 localization in A549 cells treated with IFN-γ.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
A549 cells were treated with 500 U/mL of IFN-γ for 2 h, then analyzed by immunofluorescence microscopy to assess p-STAT1 localization.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
In untreated cells, p-STAT1 was primarily detected in the cytoplasm.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Following IFN-γ treatment, increased nuclear localization of p-STAT1 was observed.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
DAPI was used for nuclear staining, and β-actin staining was used to visualize the cytoskeleton Studies reveal that IFN-γ dramatically increases the expression of PD-L1 on cancer cells, mainly by activating the STAT1 signaling pathway.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
To validate this association, we examined PD-L1 upregulation upon IFN-γ treatment in A549 cells.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Western blot analysis revealed a time-dependent increase in PD-L1 protein levels, with minimal expression in untreated control cells.
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
Upon IFN-γ stimulation, PD-L1 levels began to increase at 30 min and 1 h, corresponding with the early activation of STAT1 phosphorylation (p-STAT1, Tyr701).
PMC12141184
Curcumin inhibits IFN-γ induced PD-L1 expression via reduction of STAT1 Phosphorylation in A549 non-small cell lung cancer cells.
By 2 h, PD-L1 expression was noticeably upregulated, and by 24 h, it reached its maximum induction (p < 0.01).