PMCID string | Title string | Sentences string |
|---|---|---|
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | These findings underscore the significance of ncRNAs in autophagy regulation and drug resistance. |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | Targeting specific ncRNAs that control autophagy pathways may represent a promising strategy for enhancing GIST therapy. |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | Growing evidence suggests that ncRNAs, particularly miRNAs and lncRNAs, play crucial roles in regulating ferroptosis. |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | In tumor cells, ncRNAs influence ferroptosis by modulating genes involved in iron metabolism, antioxidant defense, and membrane lipid composition. |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | For example, miRNAs have been shown to regulate ferroptosis by targeting key genes such as GPX4, FTH1, and SLC7A11, thereby affecting tumor cell survival . |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | In gastrointestinal cancers, including gastric and colorectal cancer, miRNAs regulate ferroptosis by modulating iron homeostasis, lipid peroxidation, and oxidative stress responses . |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | miRNAs regulate ferroptosis by binding to target genes' 3' untranslated regions (3'UTRs), influencing iron balance and redox homeostasis. |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | For instance, miR-27a downregulates GPX4, a critical antioxidant enzyme suppressing lipid peroxidation. |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | Reduced GPX4 expression enhances ferroptosis and alters tumor cell proliferation and viability . |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | Similarly, miR-9 targets SLC7A11, a key component of system Xc, thereby decreasing intracellular glutathione (GSH) levels and increasing oxidative stress and iron accumulation . |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | These findings highlight the importance of miRNAs in regulating ferroptosis through direct control of iron metabolism and antioxidant capacity. |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | lncRNAs have also emerged as important regulators of ferroptosis. |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | Unlike miRNAs, lncRNAs typically modulate gene expression by interacting with transcription factors or epigenetic regulators. |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | lncRNA H19, for example, is upregulated in several cancers and influences ferroptosis by targeting miR-675 and regulating iron metabolism genes . |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | Another lncRNA, p53RRA, enhances p53 transcriptional activity, suppresses GPX4 expression, and promotes ferroptosis . |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | These mechanisms suggest that lncRNAs regulate ferroptosis by controlling oxidative stress and iron-related gene expression. |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | circRNAs, a newly identified ncRNA subtype, regulate ferroptosis primarily through miRNA sponging. |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | In gastric cancer, circ_0000284 binds to miR-29a, reducing its activity. |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | Since miR-29a inhibits FTH1, a ferroptosis suppressor, this sponging effect enhances ferroptosis . |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | Conversely, circRNA CDR1as regulates miR-7 and upregulates FTH1 expression, suppressing ferroptosis and promoting tumor growth and drug resistance . |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | These studies illustrate the dual roles of circRNAs in modulating ferroptosis, either enhancing or inhibiting the process through miRNA regulation. |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | Targeting ncRNAs presents a promising therapeutic strategy for modulating ferroptosis in cancer. |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | RNA interference and CRISPR/Cas9 technologies have enabled precise manipulation of specific miRNAs and lncRNAs, allowing selective ferroptosis induction in tumor cells. |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | For example, miRNA mimics or inhibitors can regulate ferroptosis-related genes involved in iron metabolism. |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | CRISPR-based approaches offer high specificity and the potential to fine-tune ferroptosis activation without damaging normal cells . |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | These strategies not only improve treatment efficacy but may also enhance anti-tumor immunity. |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | Overall, ncRNA-based modulation of ferroptosis opens up new avenues for precision cancer therapy. |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | PCD plays a vital role in preventing uncontrolled proliferation and malignant transformation, while its dysregulation is commonly associated with tumor progression and therapeutic resistance. |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | IM has been shown to induce autophagy, apoptosis, and ferroptosis as a first-line treatment for GIST. |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | The crosstalk among these PCD pathways significantly influences drug sensitivity and is closely linked to metastasis and recurrence. |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | This study systematically explored the regulatory roles of ncRNAs in PCD pathways in GIST, highlighting their key mechanisms in apoptosis, autophagy, and ferroptosis and their potential association with malignancy and drug resistance, thereby providing a theoretical foundation for precision therapy. |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | However, challenges remain in understanding the interactions among different ncRNAs, their roles within the tumor immune microenvironment, and developing efficient and targeted delivery strategies. |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | Future research integrating single-cell sequencing, multi-omics analysis, and functional validation is expected to further elucidate the ncRNA-PCD-GIST regulatory axis. |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | In the next few years, key directions include network-level dissection of ncRNA-PCD regulation, clinical translation of ncRNA biomarkers, development of therapeutic strategies such as ASOs and CRISPR tools, and integration of ncRNA targeting with immunotherapy to optimize treatment paradigms. |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | Despite the comprehensive analysis of ncRNA-mediated PCD regulation in GIST, several limitations should be acknowledged. |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | The study is largely based on literature synthesis and existing experimental data, lacking in vivo and in vitro validation of specific ncRNAs, making it difficult to define their direct functional roles in PCD. |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | Given the molecular heterogeneity of GIST, ncRNA expression and function may vary across different mutation subtypes, which were not fully addressed here. |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | Moreover, although we discussed ncRNAs as potential therapeutic targets, current ncRNA-based interventions in GIST remain in the early stages. |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | Efficient delivery, stability, and off-target minimization remain major barriers to clinical application. |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | Notably, the role of ncRNAs in shaping the immune microenvironment of GIST is not well understood, although PCD pathways are increasingly recognized to intersect with tumor immune regulation. |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | Future work should combine single-cell sequencing, integrative multi-omics, and functional studies to systematically unravel the molecular landscape of the ncRNA-PCD-GIST axis and identify critical regulators involved in tumor progression, immune modulation, and drug resistance. |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | Exploration of additional cell death pathways in GIST may expand the therapeutic target pool and contribute to developing a more comprehensive risk stratification model. |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | Such a model could incorporate conventional biological features and PCD-related molecular profiles to support more precise clinical decision-making. |
PMC12065685 | Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors | Identifying novel PCD-associated prognostic or predictive biomarkers and elucidating their mechanistic roles may accelerate the advancement of personalized therapy in GIST. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal neoplasms of the gastrointestinal tract. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | However, up to 40–50% of GISTs develop secondary resistance after an average of 24 months of imatinib treatment. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | It has been reported that autophagy can promote the survival of GIST cells and induce drug resistance. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | Presently, the specific mechanism of autophagy in GISTs with imatinib resistance is not clear. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | The cell-counting kit (CCK)-8 method and flow cytometry were used for in vitro drug sensitivity testing and autophagy level detection. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | Detection of the apoptosis level was by flow cytometry with the annexin V Kit. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | Western blotting was used to analyze the role of autophagy and apoptosis in GIST cells with CQ alone, imatinib alone, or in combination, and to analyze MAPK pathway expression. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | In vitro results were confirmed by in vivo experiments using the mice model. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | Hematoxylin and eosin and immunohistochemical staining were used to detect the pathological characteristics and immunophenotype of the transplanted tumor. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | Detection of KIT and PDGFRA gene mutations in the transplanted imatinib-resistant GIST was done by denaturing high performance liquid chromatography (DHPLC) and direct sequencing. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | ERK and KIT expression and regulation levels were detected by Western blotting. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | In vitro and vivo experiments, the autophagy level of imatinib-resistant cells was higher than that of normal cells; CQ combined with imatinib can promote apoptosis by blocking autophagy of imatinib-resistant cells. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | In the meanwhile, we found that the phosphorylation level of ERK may be related to autophagy. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | Our data suggest that autophagy through the MAPK/ERK pathway may play a pivotal role in imatinib-resistant GIST proliferation. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | Moreover, combining an autophagy inhibitor with imatinib may be a potential valuable strategy in overcoming acquired resistance in GIST patients. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal neoplasms of the gastrointestinal tract, accounting for 1–3% of all digestive tract tumors and almost 5% of all soft tissue sarcomas.1 With the increase in knowledge and improvement of the level of diagnosis, the incidence of GISTs is increasing year by year. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | Up to 85% of GISTs acquire mutations in the KIT gene and 3–18% in the platelet-derived growth factor receptor A (PDGFRA) gene.2 GIST responds to treatment with targeted KIT/PDGFRA inhibitors such as imatinib mesylate.3–5 However, up to 40–50% of GISTs develop secondary resistance after an average of 24 months of imatinib treatment. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | Based on the natural evolution of the disease, the patient could be placed on a higher dose of imatinib or a tyrosine kinase inhibitor such as ripretinib, though resistance can be a challenge.6–8 Resistance to imatinib has been of great interest in recent research. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | Autophagy and apoptosis are crucial and fundamental to cancer development.9 It has been reported that autophagy can promote the survival of GIST cells and induce drug resistance.10,11 Moreover, a combination of autophagy inhibitors and imatinib has achieved almost complete remission in the treatment of imatinib-resistant chronic myeloid leukemia.12,13 Inhibition of autophagy synergizes with imatinib to increase GIST cell death and retard the outgrowth of residual GIST viable cells when compared with imatinib alone therapy.14 Combining imatinib and autophagy inhibition is a potentially valuable strategy to promote GIST cytotoxicity and to diminish both cellular quiescence and acquired resistance in GIST patients.15 Presently, the specific mechanism of autophagy in GISTs with imatinib resistance is not clear. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | The PI3K/Akt/mTOR and Mitogen Activated Protein Kinase (MAPK) pathways are pivotal for cell growth and differentiation and are frequently hyperactivated during tumorigenesis (Figure 1E).16 MAPK signaling plays a critical role in the balance of apoptosis and autophagy in the response to chemotherapeutic agents.17 Activated MAPK can transmit extracellular signals to regulate cell growth, proliferation, differentiation, migration, apoptosis, etc. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | Apoptosis and macroautophagy (hereafter referred to as autophagy) can be induced by extracellular stimuli such as treatment with chemotherapeutic agents, resulting in different cell responses to these drugs. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | Figure 1(A) Effect of imatinib on drug sensitivity of GIST882 cell line. ( |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | Effect of imatinib on drug sensitivity of GIST882-ir cell line. ( |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | Effect of imatinib and chloroquine on apoptosis of GIST882-ir cell line (after 48h). ( |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | The effects of Imatinib and Chloroquine on cell viability of GIST882-ir strains after 8h, 24h and 48h. ( |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | The two essential proliferative intracellular signaling pathways, PI3K/Akt/mTOR and MAPK. ( |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | Five group Western blot results. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | 1. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | GIST882, 2. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | GIST882-ir, 3. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | GIST882-ir +im, 4. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | GIST882-ir +CQ, 5. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | GIST882-ir +im+CQ. ( |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | Effect of imatinib on drug sensitivity of GIST882 cell line. ( |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | Effect of imatinib on drug sensitivity of GIST882-ir cell line. ( |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | Effect of imatinib and chloroquine on apoptosis of GIST882-ir cell line (after 48h). ( |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | The effects of Imatinib and Chloroquine on cell viability of GIST882-ir strains after 8h, 24h and 48h. ( |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | The two essential proliferative intracellular signaling pathways, PI3K/Akt/mTOR and MAPK. ( |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | Five group Western blot results. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | 1. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | GIST882, 2. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | GIST882-ir, 3. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | GIST882-ir +im, 4. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | GIST882-ir +CQ, 5. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | GIST882-ir +im+CQ. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | Our previous research suggests the possibility of activation of the RAS-RAF-MEK-ERK pathways driven by a KIT-independent oncogenic mechanism in GISTs.18 In imatinib-resistant GISTs with both KIT V559D and BRAF V600E mutations, the inhibition of KIT V559D by imatinib caused a strong decrease of AKT phosphorylation, while ERK1/2 phosphorylation was not affected. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | The detection of alterations in the MAPK pathway in GISTs would be innovative and could be relevant in receptor tyrosine kinase inhibitor resistance or autophagy. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | Herein, we explored the role of an autophagy inhibitor, chloroquine (CQ) in imatinib-resistant GISTs and elaborated the role of the MAPK/ERK pathway in autophagy inhibition. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | GIST882 cell lines, GIST882 imatinib-resistant cell lines, GIST882 cell mice, GIST imatinib-resistant cell mice. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | GIST882: normal control group; GIST882-ir: imatinib-resistant cell lines; GIST882-ir +im: imatinib-resistant cell lines + imatinib; GIST882-ir +CQ: imatinib-resistant cell lines + chloroquine; GIST882-ir +im+ CQ: imatinib-resistant cell lines + imatinib + chloroquine. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | The above imatinib-resistant cell lines and GIST882 were inoculated into nude mice to observe their tumorigenicity. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | The tumor size, growth rate, and survival time of nude mice were observed. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | Forty 4–5 weeks old, 16–18 g, and specific pathogen-free NOD/SCID male mice were purchased from the Shanghai Slyke Laboratory Animal Limited Liability Company (license number: SCXK (Shanghai) 2013–0018, certification number: 0301907). |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | The quality of drinking water was in accordance with the national standard of the People’s Republic of China (GB5749-2006). |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | The license number of the laboratory animal room was SYXK (zhejiang) 2015–0008. |
PMC7342409 | Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway | The temperature and relative humidity of the feeding environment ranged from 20–25 °C and 40–70%, respectively. |
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