ArticleCancer biology & therapy2018
RNF138 confers cisplatin resistance in gastric cancer cells via activating Chk1 signaling pathway.
Article in Cancer biology & therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 22 citations in OpenAlex.
- Ubiquitination mediated by RING-type E3 ligases in the progression of digestive system tumors: mechanistic insights and potential therapeutic strategies.Frontiers in cell and developmental biology · 2026Review
- The enigma of the RING-UIM E3 ligases: its transformative impact on cancer research.Journal of translational medicine · 2025Review
- RNF138 contributes to cisplatin resistance in nasopharyngeal carcinoma cells.Scientific reports · 2025Article
- Platinum-based metal complexes as chloride transporters that trigger apoptosis.Chemical science · 2024Article
- An innovative prognostic auxiliary for colon adenocarcinoma based on zinc finger protein genes.Translational cancer research · 2024Article
- RNF138 Downregulates Antiviral Innate Immunity by Inhibiting IRF3 Activation.International journal of molecular sciences · 2023Article
- Mechanism of cisplatin resistance in gastric cancer and associated microRNAs.Cancer chemotherapy and pharmacology · 2023Review
- Ubiquitin E3 ligases in cancer: somatic mutation and amplification.BMB reports · 2023Review
- Fibroblast growth factor signalling influences homologous recombination-mediated DNA damage repair to promote drug resistance in ovarian cancer.British journal of cancer · 2022Article
- RING finger 138 deregulation distorts NF-кB signaling and facilities colitis switch to aggressive malignancy.Signal transduction and targeted therapy · 2022Article
- SIAH1 reverses chemoresistance in epithelial ovarian cancer via ubiquitination of YBX-1.Oncogenesis · 2022Article
- Glaucocalyxin A suppresses multiple myeloma progression in vitro and in vivo through inhibiting the activation of STAT3 signaling pathway.Cancer cell international · 2021Article
- Silencing microRNA‑29b‑3p expression protects human trabecular meshwork cells against oxidative injury via upregulation of RNF138 to activate the ERK pathway.International journal of molecular medicine · 2021Article
- A Gene-Expression Predictor for Efficacy of Induction Chemotherapy in Locoregionally Advanced Nasopharyngeal Carcinoma.Journal of the National Cancer Institute · 2021Article
- Roles of E3 ubiquitin ligases in gastric cancer carcinogenesis and their effects on cisplatin resistance.Journal of molecular medicine (Berlin, Germany) · 2021Review
- LncRNA HLA Complex Group 11 Knockdown Alleviates Cisplatin Resistance in Gastric Cancer by Targeting the miR-144-3p/UBE2D1 Axis.Cancer management and research · 2021Article
- E3 Ubiquitin Ligase in Anticancer Drugdsla Resistance: Recent Advances and Future Potential.Frontiers in pharmacology · 2021Review
Corrections and comments
- Erratum issuedCorrection.2024
Authors and funding
15 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chemotherapy resistance represents a major issue associated with gastric cancer (GC) treatment, and arises through multiple mechanisms, including modulation of the cell-cycle check point. Several ubiquitin kinases, including RING finger protein 138 (RNF138), have been reported to mediate the G2/M phase arrest. In this study, we investigated the role of RNF138 in the development of cisplatin resistance of two GC cell lines. We show that RNF138 levels are higher in cisplatin-resistant cell lines, compared with cisplatin-sensitive cells, and RNF138 expression was elevated during drug withdrawal following the cisplatin treatment. Using gene overexpression and silencing, we analyzed the impact of altering RNF138 level on GC cell viability, apoptosis, and cell cycle phenotypes in two isogenic cisplatin-sensitive and resistant cell lines. We show that RNF138 overexpression increased GC cell viability, decreased apoptosis and delayed cell cycle progression in the cisplatin-sensitive GC cells. Conversely, RNF138 silencing produced opposite phenotypes in the cisplatin-resistant cells. Moreover, RNF138-dependent phosphorylation of Chk1 was seen in GC cells, indicating a novel connection between cisplatin-induced DNA damage and apoptosis. Collectively, these data suggest that RNF138 modulates the cisplatin resistance in the GC cells, thus serving as a potential drug target to challenge chemotherapy failure. In addition, RNF138 can also be used as a marker to monitor the development of cisplatin resistance in GC treatment.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.