PMCID string | Title string | Sentences string |
|---|---|---|
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Moreover, the usefulness of F-Fluorodeoxyglucose positron emission tomography/computed tomography (FDG PET/CT) and findings about the glycolytic system as a biomarker in GIST are presented. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | For details, please refer to sections from Glucose transporter (GLUT) to Biomarkers. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Fig 1 A schematic illustration of the relationship between gastrointestinal stromal tumor (GIST) and glycolysis and oxidative phosphorylation (OXPHS). |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Particularly, we focused on the relationship bwtween GIST and imatinib, a representative drug for treating GIST. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Moreover, the usefulness of F-Fluorodeoxyglucose positron emission tomography/computed tomography (FDG PET/CT) and findings about the glycolytic system as a biomarker in GIST are presented. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | For details, please refer to sections from Glucose transporter (GLUT) to Biomarkers. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | EVs: extracellular vesicles; GLUT: glucose transporter; HK1: hexokinase 1; PKM2: pyruvate kinase M2; LDH: lactate dehydrogenase; MCT: monocarboxylate transporter; MTV: metabolic tumor volume; PFS: progression-free survival: RFS: recurrence-free survival; SUVbsa: standardized uptake value corrected for body surface area; SUVbw: standardized uptake value corrected for body weight; SUVlbm: standardized uptake value corrected for lean body mass; TLG: total lesion glycolysis Considering substantial evidence regarding lactate and altered cellular metabolism in various cancers, targeting these aspects is now a major focus for pharmaceutical drug development . |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | While research has highlighted the effectiveness of glycolysis pathway inhibitors in various cancer types and their anti-GIST potential is being explored, several aspects remain unclear . |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | GLUT inhibitors have started being increasingly recognized for their potential to target glucose dependency in cancer and other diseases, thereby opening new avenues for future drug development . |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Our research indicated that WZB117 induced apoptosis in imatinib-resistant GIST cells . |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | To the best of our knowledge, no other studies have reported on the association between GLUT inhibitors and GIST. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Gossypol, a recognized LDHA inhibitor, and 3-bromopyruvate (3-BP), an inhibitor of HK2, have demonstrated efficacy against specific imatinib-resistant GIST cell lines. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | However, the mechanism underlying these cell growth suppressions is yet to be elucidated . |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | 2-deoxyglucose (2DG), an HK inhibitor, has been identified as a potential agent for treating tumors . |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | While an in vitro study has demonstrated that 2DG possesses significant disease-specific effects, its primary action in GIST is not the disruption of energy production through glycolysis inhibition. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | 2DG primarily functions by inhibiting KIT through suppression of KIT glycosylation . |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Targeting MCT has emerged as a potential therapeutic strategy in cancer. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Pharmacological and genetic suppression of MCT1 or MCT4 lead to reduced tumor cell proliferation in vitro and in vivo, making them promising therapeutic targets . |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | While the efficacy of MCT inhibitors has been indicated in several types of tumors , there is currently no evidence supporting their anti-GIST efficacy. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | As shown in Fig. 2, it is noteworthy that very few reports have demonstrated the efficacy of drugs targeting the glycolytic system in GIST.Fig. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | 2A schematic representation of aerobic glycolysis and its inhibitors in gastrointestinal stromal tumor (GIST) cells. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | The three drugs (WZB117, 3-BP, and Gossypol) inhibit glucose transporter (GLUT), hexokinase 2 (HK2), and lactate dehydrogenase (LDH), respectively. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Only these three glycolytic inhibitors are potentially effective against GISTs. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Note: 2-Deoxyglucose (2DG) serves as an HK inhibitor; however, its principal action within GIST does not primarily involve the curtailment of energy generation through inhibition of glycolysis. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Instead, it mainly operates through repression of KIT by suppressing KIT glycosylation. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Fig 2 A schematic representation of aerobic glycolysis and its inhibitors in gastrointestinal stromal tumor (GIST) cells. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | The three drugs (WZB117, 3-BP, and Gossypol) inhibit glucose transporter (GLUT), hexokinase 2 (HK2), and lactate dehydrogenase (LDH), respectively. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Only these three glycolytic inhibitors are potentially effective against GISTs. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Note: 2-Deoxyglucose (2DG) serves as an HK inhibitor; however, its principal action within GIST does not primarily involve the curtailment of energy generation through inhibition of glycolysis. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Instead, it mainly operates through repression of KIT by suppressing KIT glycosylation. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | 2PG: 2-phosphoglycerate; 3-BP: 3-bromopyruvate; ENO: enolase; Fructose 6-P: fructose-6-phosphate; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; Glucose 6-P: glucose-6-phosphate; LDH: lactate dehydrogenase; MCT: monocarboxylate transporter; PEP: phosphoenolpyruvate; PFK: phosphofructokinase; PK: pyruvate kinase As discussed in this review, the critical association between GIST and glycolysis is yet to be fully elucidated. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Given the rarity of GIST and the limited treatment options currently available, there is a compelling need for further exploration of the association between GIST and glycolysis. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Such investigations can potentially unveil novel anti-GIST therapeutic strategies in the future. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Furthermore, the mechanism of imatinib resistance should be clarified from the perspective of the glycolytic system and strategies to overcome imatinib resistance should be developed. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Glycolysis inhibition represents a promising target for therapeutic development. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Despite several key molecules in the glycolysis pathway, only three glycolytic inhibitors exhibit potential anti-GIST efficacy. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Furthermore, differences exist among effective inhibitors depending on the metabolic phenotype of the cell lines. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Further studies are required to substantiate these findings and establish the effectiveness of glycolysis inhibitors as potential anti-GIST therapeutic targets. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | This review discusses the involvement of glycolysis-related molecules in the pathogenesis of GIST and their potential as therapeutic targets. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | It also explores prospects for GIST research within glycolysis. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Targeting glycolysis as a therapeutic approach shows significant promise as a novel strategy for GIST treatment. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | The insights gained from the reviewed reports hold the potential to lead to significant advancements in the field of GIST treatment. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Takafumi Shima: Data curation, Investigation, Writing – original draft. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Kohei Taniguchi: Writing – review & editing. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Yosuke Inomata: Writing – review & editing. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Jun Arima: Writing – review & editing. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | Sang-Woong Lee: Writing – review & editing. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | The author is not an Editorial Board Member/Editor-in-Chief/Associate Editor/Guest Editor for Neoplasia and was not involved in the editorial review or the decision to publish this article. |
PMC11261875 | Glycolysis in gastrointestinal stromal tumor: a brief overview | The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: none |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | Imatinib (IM) has significantly improved the prognosis of gastrointestinal stromal tumor (GIST) patients, but some patients still have primary resistance to IM, and approximately half of patients develop acquired drug resistance within 2 years of treatment, necessitating exploration of new treatment strategies. |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | Targeting ferroptosis as a novel approach to tumor treatment has gained attention. |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | Yet, there is limited research on ferroptosis in GIST, and the underlying mechanism remains unclear. |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | In this study, we revealed that IM increased lipid reactive oxygen species and intracellular Fe levels, and decreased glutathione levels in GIST. |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | This effect could be partially inhibited by Ferrostatin-1. |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | Additionally, knocking down STUB1 and overexpressing GPX4 reversed the IM-induced ferroptosis effect. |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | Moreover, STUB1 was identified as a novel E3 ubiquitin ligase of GPX4, promoting the ubiquitination at site K191 of GPX4. |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | The combination of the GPX4 inhibitor RSL3 and IM synergistically induces ferroptosis, inhibiting GIST proliferation both in vivo and in vitro. |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | Furthermore, STUB1 and GPX4 expression serve as independent prognostic factors for GIST. |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | In conclusion, This study is the first to demonstrate that IM induces ferroptosis by promoting STUB1-mediated GPX4 ubiquitination in GIST, and the combination of RSL3 and IM emerges as a promising therapeutic strategy for GIST.Gastrointestinal stromal tumor (GIST) is the most common tumor of mesenchymal origin in the gastrointestinal tract, with an annual incidence of 1/100,000–2/100,000 . |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | C-kit mutations are detected in 75%-80% of patients, whereas platelet-derived growth factor receptor alpha (PDGFRA) gene mutations only account for 5%-10% . |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | Early diagnosis of GIST is often difficult. |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | Surgical resection remains the most effective treatment, but recurrence and metastasis often occur postoperatively. |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | In addition, GIST is insensitive to radiotherapy and chemotherapy, making the prognosis poor. |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | Although the emergence of tyrosine kinase inhibitors (TKIs) has significantly improved the prognosis of GIST patients, including Imatinib (IM) as the first-line treatment for recurrent, metastatic, and unresectable GIST , about 50% of GIST patients may develop acquired drug resistance within 2 years of treatment . |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | Although TKIs have been developed to the fourth generation, acquired drug resistance remains a problem. |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | As a result, the overall treatment outcome of GIST remains unsatisfactory, and the latest clinical and basic research has focused on the new therapeutic targets . |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | Ferroptosis, a regulated cell death caused by fatal lipid peroxidation was proposed by Dixon in 2012 . |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | Subsequent studies identified lipid peroxidation as a key factor triggering membrane oxidative damage during ferroptosis . |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | Lipid peroxides are the result of oxidative damage to polyunsaturated fatty acids (PUFAs) caused by reactive oxygen species (ROS). |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | This oxidative damage can disrupt the lipid bilayer and impact membrane function, ultimately leading to ferroptosis . |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | Inside the cell, the clearance of lipid peroxides primarily relies on the activity of the antioxidant enzyme glutathione peroxidase 4 (GPX4). |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | GPX4 utilizes glutathione (GSH) as a substrate to convert lipid peroxides into normal phospholipid molecules. |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | The synthesis of GSH is contingent on the availability of intracellular cysteine, which can be generated from cystine imported from the extracellular space via the cysteine-glutamate antiporter (Systemxc-, composed of recombinant solute carrier family 7, member 11, SLC7A11, and recombinant solute carrier family 3, member 2, SLC3A2) . |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | Because GPX4 is the sole cellular enzyme capable of reducing lipid peroxides to lipids, it plays a critical role in ferroptosis and serves as the target for various ferroptosis inducers . |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | A variety of tumors have been reported to be associated with ferroptosis, and targeting ferroptosis against tumor development and progression has become a promising approach in tumor therapy . |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | Several drugs have been identified to act through ferroptosis induction in different tumors, mainly including Systemxc- inhibitors (Erastin, sulfasalazine, sorafenib), glutathione depletion factor (FIN56), and GPX4 inhibitors (RSL3). |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | Notably, sulfasalazine and sorafenib have received approval from the US Food and Drug Administration (FDA) for clinical use [12–16]. |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | However, the existence of ferroptosis in GIST and its mechanism remain unclear. |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | The ubiquitin-proteasome pathway regulates target protein degradation, involving ubiquitin-activating enzyme 1 (E1), ubiquitin-conjugating enzyme 2 (E2) and ubiquitin ligase enzyme 3 (E3). |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | Dysfunctional ubiquitin E3 ligase expression determines ubiquitination specificity and rate-limiting steps, playing a crucial role in tumor development . |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | STUB1, also known as the C terminus of HSP 70 interacting protein (CHIP), contains a tetratricopeptide repeat and a U-box, which is a ubiquitin E3 ligase targeting various oncogene-encoded proteins (such as p53, c-Myc, PTEN, AR-V7, and EGFR) [19–22]. |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | This study is the first to demonstrate that IM induces ferroptosis by promoting STUB1-mediated GPX4 ubiquitination in GIST and identify STUB1 as a novel ubiquitin E3 ligase targeting GPX4. |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | Moreover, we demonstrate the synergistic effect of IM combined with RSL3 in treating GIST, suggesting that inhibiting GPX4 to induce ferroptosis could enhance GIST therapy. |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | GIST-T1 cell line was purchased from Cosmo Bio Co. Ltd. (Tokyo, Japan) and GIST-882 cell line was provided by Dr. Fletcher of Harvard Medical School. |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | Both cell lines were verified by short tandem repeat (STR) profiling and tested negative for mycoplasma contamination. |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | Human GIST cell lines (GIST-T1 and GIST-882) were cultured in Iscove’s Modified Dulbecco Medium (IMDM, Corning, #10–016-CV, USA) and RPMI 1640 medium (Gibco, #11875119, USA) supplemented with 10% fetal bovine serum (FBS, Gibco, #10099141C, USA) and 1% penicillin-streptomycin (Gibco, #15140122, USA). |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | Cells were passaged at 70%–80% confluence by dissociation from plates using 0.25% Trypsin-EDTA (Gibco, #25200056, USA). |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | All cells were incubated in a 37°C incubator (Forma, USA) containing 5% CO2. |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | The cells were seeded in a 96-well plate with 2 × 10 cells and 100 µl medium per well. |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | After culturing for some time, the medium was replaced with 100 µl medium with 10 µl cell counting kit-8 (#40203ES76, CCK-8, Yeasen, China). |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | After 2 hours, the 96-well plate was oscillated for 2 min. |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | The absorbance value was detected with a microplate reader (Thermo Fisher, USA) at 450 nm. |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | Three replicate wells were run in each experiment, and each experiment was repeated three times. |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | The cell viability results were normalized to the number of cells in the control group. |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | Drug inhibition assay was performed by seeding and incubating 5 × 10 GIST-T1 or GIST-882 cells at 37 °C overnight. |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | Cells were treated with RSL3 and IM at various doses, and the half-maximal inhibitory concentration assay (IC50) was calculated using nonlinear regression analysis in GraphPad Prism 8.0.2. |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | The synergistic effect of the combination treatment was measured using CompuSyn software (Paramus, NJ, USA). |
PMC10728200 | Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination | The combination index (CI) >1, =1, and <1 indicate antagonistic, additive, or synergic effects, respectively. |
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