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PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
n = 3 mice per group.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
G Immunohistochemical staining representative pictures of hematoxylin-eosin (HE), KIT, STUB1, GPX4, Ki-67, and 4-HNE in GIST cell xenograft tumor tissues of mice from vehicle (DMSO), IM, RSL3, and combination treatment groups.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
Scale bar, 100 μm.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
DMSO dimethyl sulfoxide, IM Imatinib, RSL3 Ras-selective lethal small molecule 3, 4-HNE 4-hydroxy-2-nonenal.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
Significance denoted by: ns not significant, *P < 0.05, **P < 0.01, and ***P < 0.001.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
Based on the staining intensity of STUB1 and GPX4 (Fig. 7A), IHC analysis of 418 tissue microarray samples revealed that there was a significant inverse correlation between the expression of STUB1 and GPX4 in GIST (Fig. 7B).
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
Subsequently, correlations between STUB1 and GPX4 expression and clinicopathological features in the 418 patients with GIST were analyzed.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
The results showed that STUB1 expression was correlated with tumor location (P < 0.001), mitotic index (P < 0.001), NIH risk grade (P = 0.001), and cell morphology (P = 0.047).
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
The expression of GPX4 was correlated with tumor location (P = 0.020), mitotic index (P = 0.019) and NIH risk grade (P = 0.005) (Table S4).
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
The survival and recurrence status were last updated in August 2022.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
Among the 418 included patients, 397 patients (95.0%) were followed up completely and 21 were lost to follow-up.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
The median follow-up period was 48 (0–86) months.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
At the last follow-up, recurrence occurred in 34 cases (8.1%) and death in 4 (1.0%) cases.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
The overall 3- and 5-year recurrence-free survival(RFS) rate was 93.3% and 90.9% respectively.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
Log-rank analysis revealed significantly longer RFS in patients with high expression of STUB1 (P = 0.034) and low expression of GPX4 (P = 0.004; Fig. 7C, D).
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
but there was no significant difference in overall survival(OS) (Fig. S9).Fig.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
7STUB1 and GPX4 are independent prognostic factors for gastrointestinal stromal tumor (GIST).A Immunohistochemical analysis for the STUB1 and GPX4 expression in GIST tissue microarrays (n = 418).
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
B Scatter plot showing a negative correlation between the expression of STUB1 and GPX4 in GIST.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
C Low STUB1 expression predicted poor recurrence-free survival (RFS) in GIST patients.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
D High GPX4 expression predicted poor RFS in GIST patients.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
E Nomogram for predicting the probability of recurrence in patients with GIST.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
F Calibration plot of the nomogram.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
Scale bar, 50 μm in A. A Immunohistochemical analysis for the STUB1 and GPX4 expression in GIST tissue microarrays (n = 418).
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
B Scatter plot showing a negative correlation between the expression of STUB1 and GPX4 in GIST.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
C Low STUB1 expression predicted poor recurrence-free survival (RFS) in GIST patients.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
D High GPX4 expression predicted poor RFS in GIST patients.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
E Nomogram for predicting the probability of recurrence in patients with GIST.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
F Calibration plot of the nomogram.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
Scale bar, 50 μm in A. Univariate Cox analysis indicated that RFS was correlated with mitotic index (P < 0.001), cell morphology (P < 0.001), STUB1 expression (P = 0.039), and GPX4 expression (P = 0.006) (Table S5).
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
The results of multivariate Cox analysis showed that mitotic index > 5/50HPF (HR: 3.907, 95%CI: 1.838–8.305, P < 0.001), epithelial and mixed cell type (HR: 2.179, 95%CI: 1.013–4.685, P = 0.046) and high GPX4 expression (HR: 5.806, 95%CI: 2.349–14.353, P < 0.001) were independent risk factors for recurrence (Table S5).
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
The high expression of STUB1 (HR: 0.370, 95%CI: 0.172–0.794, P = 0.011) was an independent protective factor affecting the RFS of GIST patients.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
However, there was no correlation between OS and various factors (Table S6).
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
Multivariate analysis was used to create a nomogram for survival prediction, and it was observed that compared to other clinical variables, STUB1 and GPX4 expression had a significant impact on RFS (Fig. 7E).
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
The calibration plot showed good consistency between predicted and observed values, as the deviation correction line closely matched the ideal curve (45-degree line) (Fig. 7F).
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
In summary, a valuable model for predicting recurrence in patients with GIST has been constructed.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
The emergence of TKIs has improved the prognosis of GIST patients, however, approximately half of the patients develop acquired drug resistance due to secondary gene mutations within 2 years of treatment, which hinders the effectiveness of TKI treatment .
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
Therefore, exploring new treatment strategies is imperative.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
Ferroptosis, a novel form of cell death has garnered significant attention .
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
Eliminating tumors by targeting ferroptosis could be a potential therapeutic option for GIST.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
However, the role of ferroptosis in the tumorigenesis and progression of GIST and whether IM can induce ferroptosis remain unclear.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
In this study, we first detected the presence of ferroptosis in GIST-T1 and GIST-882 cells and found that inhibition of ferroptosis by Ferrostatin-1 partially reversed the effect of IM on GIST, indicating that ferroptosis does exist in GIST.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
The detection indexes of ferroptosis include the changes in mitochondrial morphology and levels of lipid ROS, Fe, and GSH .
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
We observed a reduction in mitochondrial volume and an increase in mitochondrial crests in GIST cells treated with IM.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
IM increased ROS and lipid ROS levels in GIST cells, and this effect could be reversed by Ferrostatin-1.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
In addition, IM promoted the accumulation of Fe in GIST and decreased the GSH/GSSG ratio in a concentration-dependent manner.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
These results suggest that IM induces ferroptosis in GIST cells.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
The mechanism of ferroptosis primarily involves classical pathways dependent on cysteine-glutamate antiporter (Systemxc-, is composed of SLC7A11 and SLC3A2) and GPX4 [34–36], and non-classical pathways such as abnormal lipid peroxide metabolism and iron metabolism .
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
To clarify the specific molecular mechanism of IM-induced ferroptosis, we examined the effects of different IM concentrations and treatment durations on the expression of SLC7A11, GPX4, acyl-CoA synthetase long-chain family member 4 (ACSL4), ferritin-heavy polypeptide 1 (FTH1) and transferrin receptor 1 (TFR1) at the transcriptional level.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
Our results indicated no significant effect on the expression of ACSL4 (Fig. S10).
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
The up-regulation of FTH1 and down-regulation of TFR1 may be caused by negative feedback (Fig. S10).
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
Therefore, we hypothesize that the mechanism of ferroptosis caused by IM may be through the classical ferroptosis pathway mediated by GSH, and this speculation was later confirmed by the significant decrease of GSH/GSSG ratio after IM treatment.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
SLC7A11 and GPX4 are the two most critical molecules in the classical ferroptosis pathway , in which no significant change was observed in the transcriptional and protein levels of SLC7A11, while GPX4 was significantly increased at the transcriptional level but significantly decreased at the protein level.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
These findings suggest that IM may regulate GPX4 expression through post-transcriptional modification.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
In addition, we found that IM increased the GPX4 mRNA levels, but this effect disappeared after adding proteasome inhibitor MG132, so we speculated that IM-induced GPX4 protein degradation may increase GPX4 mRNA levels through negative feedback (Figs. S11 and S12).
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
Interestingly, we found that RSL3 could lead to inhibition of GPX4 transcripts as well (Fig. S11).
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
This observation suggests that RSL3 might influence GPX4 at multiple levels, potentially leading to a complex regulatory response.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
One possibility is that RSL3, by inhibiting GPX4 activity and leading to lipid peroxidation, triggers a cellular stress response that results in alterations in gene expression, including GPX4 mRNA.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
It is also possible that RSL3 has indirect effects on GPX4 regulation, possibly through signaling pathways or transcription factors that control GPX4 expression.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
Further studies are needed to fully elucidate the mechanisms underlying the impact of RSL3 on GPX4 mRNA levels and to better understand the intricate regulatory networks involved in ferroptosis.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
The glutathione peroxidase protein family (GPXs) is an important protein for cells to resist peroxidation.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
GPX4 is the sole lipid peroxidation-reducing GPXs, capable of converting lipid peroxidation bonds into hydroxyl groups, thereby nullifying peroxidation activity and preventing the buildup of lipid peroxides.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
GPX4 serves as a key negative regulator of ferroptosis, with the loss of GPX4 enzyme activity being the primary cause of ferroptosis.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
Enhancing the inhibition of GPX4 expression or activity represents a novel strategy to augment ferroptosis effects.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
As a widespread post-translational modification, ubiquitin plays a vital role in biological regulation .
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
We further detected the ubiquitination level of GPX4 after IM treatment and found that IM could promote the ubiquitination of GPX4.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
Although the role of post-translational modification in ferroptosis has been gradually emphasized in recent years , it has been found that SOCS2-enhanced ubiquitination of SLC7A11 promotes ferroptosis in hepatocellular carcinoma , and ubiquitin-specific protease 7 (USP7) promotes ferroptosis via activation of the p53/TFR1 pathway , and NEDD4 ubiquitylates VDAC2/3 to suppress erastin-induced ferroptosis in melanoma .
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
However, the research on GPX4 ubiquitin is very limited .
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
To explore the specific molecules that mediate the ubiquitination of GPX4 induced by IM, we performed UbiBrowser website and found that STUB1 may be the E3 ubiquitin ligase of GPX4.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
Our subsequent DRUGSURV database analysis also showed that STUB1 may be the indirect target of IM, and that IM could upregulate STUB1 expression, and knockdown of STUB1 effectively blocked the ferroptosis induced by IM.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
We subsequently investigated the specific mechanism by which STUB1 regulates GPX4.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
As a ubiquitin ligase, STUB1 functions by binding to substrates, promoting substrate degradation.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
Currently, HMGB1 , ErbB2 and CIB1 have been identified as the substrates of STUB1.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
Ubiquitin primarily regulates target proteins through covalent binding with substrate lysines.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
However, whether STUB1 regulates GPX4 through a similar lysine-related mechanism requires further investigation.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
In the present study, CO-IP results indicated that STUB1 inhibits GPX4 protein stability and promotes GPX4 ubiquitination through direct binding to GPX4.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
We constructed GPX4 deubiquitination point mutant plasmids (K107R, K126R, K162R, K167R, K191R).
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
Immunoprecipitation results revealed that ubiquitin levels of GPX4 significantly decreased following deubiquitination mutation at K191, with concurrent inhibition of GPX4 ubiquitination mediated by STUB1.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
This suggests that K191 is a key regulatory site for GPX4 ubiquitin modification catalyzed by STUB1.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
Additionally, exploring more substrates could enhance our understanding of STUB1’s functions.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
Apart from the GSH transport system, ferroptosis is regulated by ferroptosis suppressor protein 1 (FSP1).
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
FSP1 is a NAD(P)H-ubiquinone reductase, capable of reducing vitamin K to hydroquinone, a potent free radical trapping antioxidant, and an inhibitor of (phosphorus) lipid peroxidation.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
FSP1-dependent non-classical vitamin K cycling cooperates with GPX4 and glutathione to suppress lipid peroxidation and ferroptosis .
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
Whether STUB1 can regulate FSP1 requires further exploration.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
In summary, our data suggest that IM in GIST promotes the ubiquitination at site K191 of GPX4 by promoting the expression of STUB1, resulting in the degradation of GPX4 protein and induction of ferroptosis.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
Previous studies have demonstrated that the efficacy of IM depends on the type of gene mutation, with patients harboring c-kit exon 11 mutations being more sensitive to IM than those with PDGFRA exon 18 D842V mutations .
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
Our study highlights that IM could induce ferroptosis in GIST through GPX4, yet GPX4 expression is heterogeneous in patients with GIST.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
The expression of GPX4 was found to be negatively correlated with the prognosis of GIST.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
Generally, GIST patients with high expression of GPX4 may benefit more from IM treatment.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
Further elucidating the potential mechanism of STUB1 and GPX4 in GIST and screening new drug combinations based on IM could represent a promising strategy for the treatment of GIST in the future.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
RSL3 is a specific inhibitor of GPX4 approved by the FDA, which has been shown to inhibit the growth, invasion, and metastasis of multiple cancers .
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
Our data indicate that RSL3 and IM could synergistically inhibit the expression of GPX4 and promote ferroptosis both in vivo and in vitro.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
Consequently, RSL3 demonstrates effective anti-tumor activity against GIST, and when combined with IM, it may offer additional treatment options for patients with GIST with poor responses to IM.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
However, it is important to acknowledge that our study has certain limitations.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
Specifically, the use of immunodeficient BALB/c nude mice may restrict the generalizability of our findings to the broader context of ferroptosis’s impact on the immune system.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
This encompasses aspects such as the immune tolerance of late-stage ferroptotic cancer cells and the immunogenicity of early-stage ferroptotic cancer cells.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
As pictorially modeled in Fig. 8, this study for the first time demonstrates that IM induces ferroptosis in GIST by promoting STUB1-mediated GPX4 ubiquitination, offering a novel mechanism for the inhibition of GIST.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
Furthermore, combining IM with RSL3 presents a promising therapeutic strategy for GIST.Fig.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
8Mechanism diagram of imatinib (IM) inducing ferroptosis.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
IM upregulates STUB1 expression.
PMC10728200
Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination
STUB1 overexpression promotes the ubiquitination of GPX4, thereby inducing ferroptosis in gastrointestinal stromal tumors (GIST).