ArticleBritish journal of cancer2018
The mechanism study of lentiviral vector carrying methioninase enhances the sensitivity of drug-resistant gastric cancer cells to Cisplatin.
Article in British journal of cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 26 citations in OpenAlex.
- Molecular roles of microRNA-21 and exosomal miR-21 in gastrointestinal cancers: diagnostic, therapeutic, and drug resistance insights.Frontiers in molecular biosciences · 2025Review
- Methionine restriction promotes the polarization of macrophages towards M1 and the immunotherapy effect of PD-L1/PD-1 blockades by inhibiting the secretion of MIF by gastric carcinoma cells.Translational oncology · 2025Article
- Deprivation of methionine inhibits osteosarcoma growth and metastasis via C1orf112-mediated regulation of mitochondrial functions.Cell death & disease · 2024Article
- The Role of Methionine Restriction in Gastric Cancer: A Summary of Mechanisms and a Discussion on Tumor Heterogeneity.Biomolecules · 2024Review
- Upregulation of E-cadherin by the combination of methionine restriction and HDAC2 intervention for inhibiting gastric carcinoma metastasis.Acta biochimica et biophysica Sinica · 2024Article
- H1Innovative approaches to combat anti-cancer drug resistance: Targeting lncRNA and autophagy.Clinical and translational medicine · 2023Review
- Molecular mechanisms underlying the action of carcinogens in gastric cancer with a glimpse into targeted therapy.Cellular oncology (Dordrecht, Netherlands) · 2022Review
- Wentilactone A Reverses the NF-κB/ECM1 Signaling-Induced Cisplatin Resistance through Inhibition of IKK/IκB in Ovarian Cancer Cells.Nutrients · 2022Article
- Identification and verification of the role of crucial genes through which methionine restriction inhibits the progression of colon cancer cells.Oncology letters · 2022Article
- microRNA-21: a key modulator in oncogenic viral infections.RNA biology · 2021Review
- METase/lncRNA HULC/FoxM1 reduced cisplatin resistance in gastric cancer by suppressing autophagy.Journal of cancer research and clinical oncology · 2019Article
- Research Progress in microRNA-Based Therapy for Gastric Cancer.OncoTargets and therapy · 2019Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTo investigate the mechanism of lentiviral vector carrying methioninase enhances the sensitivity of drug-resistant gastric cancer cells to Cisplatin.
methodsDeath receptors, anti-apoptotic protein, NF-κB, and TRAIL pathway-related factors were detected. The influence of LV-METase transfection on cell viability and pathway-related proteins were assessed by MTT method and western blot, respectively. Different treatments (NF-κB or caspase-3 inhibitor induction, TRAIL supplement, etc.) were performed in gastric cancer cells and the above parameters were analysed. Moreover, the connection between miR-21 and NF-κB or caspase-8 was determined by Chip and luciferase assay, respectively. LV-METase transfection drug-resistant gastric cancer cells were injected subcutaneously into mice.
resultsThe expression of free MET, miR-21-5p, MDR1, P-gp, and DR5 was significantly increased in drug-resistant gastric cancer cell lines. When cells were transfected with LV-METase, intracellular TRAIL signalling was activated while NF-κB pathway was inhibited. Besides, enhanced TRAIL signalling or repressed NF-κB pathway can promote the sensitivity of drug-resistant strains to Cisplatin, and the combination shows more sensitive to sensitisation. LV-METase promoted TRAIL expression by reducing NF-κB, thereby contributing to the downregulation of P-gp and enhancing the susceptibility of drug-resistant gastric cancer cells to Cisplatin. Furthermore, miR-21 regulated by NF-κB mediated the expression of P-gp protein via inhibiting caspase-8, thus regulating Cisplatin-induced cell death.
conclusionsOur results suggest that LV-METase has potential as a therapeutic agent for gastric cancer treatment.
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