ArticleOncology letters2021
MCM3AP-AS1 promotes cisplatin resistance in gastric cancer cells via the miR-138/FOXC1 axis.
Article in Oncology letters, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- LncRNA MCM3AP-AS1 promotes chemoresistance in triple-negative breast cancer through the miR-524-5p/RBM39 axis.Molecular and cellular biochemistry · 2025Article
- Evaluation of Long Non-coding RNA (LncRNA) in the Pathogenesis of Chemotherapy Resistance in Cervical Cancer: Diagnostic and Prognostic Approach.Molecular biotechnology · 2024Review
- Overexpression of Long Non-coding RNAsAdvanced biomedical research · 2024Article
- A review on the role of MCM3AP-AS1 in the carcinogenesis and tumor progression.Cancer cell international · 2022Review
- Non-coding RNA in cancer drug resistance: Underlying mechanisms and clinical applications.Frontiers in oncology · 2022Review
- Long Non-Coding RNA in Gastric Cancer: Mechanisms and Clinical Implications for Drug Resistance.Frontiers in oncology · 2022Review
- Contribution of MicroRNAs in Chemoresistance to Cisplatin in the Top Five Deadliest Cancer: An Updated Review.Frontiers in pharmacology · 2022Review
- Long Non-Coding RNA MCM3AP-AS1: A Crucial Role in Human Malignancies.Pathology oncology research : POR · 2022Review
- Differential Expression of Long Noncoding RNAs in Patients with Coronary Artery Disease.Molecular syndromology · 2021Article
- Therapeutically Targeting Cancers That Overexpress FOXC1: A Transcriptional Driver of Cell Plasticity, Partial EMT, and Cancer Metastasis.Frontiers in oncology · 2021Review
- MCM3AP-AS1: An Indispensable Cancer-Related LncRNA.Frontiers in cell and developmental biology · 2021Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The dysregulation of long non-coding RNAs (lncRNAs) serves a pivotal role in the pathogenesis and development of multiple types of human cancer, including gastric cancer (GC). MCM3AP-antisense 1 (MCM3AP-AS1) has been reported to function as a tumor promoter in various types of cancer. However, the biological function of MCM3AP-AS1 in the resistance of GC cells to cisplatin (CDDP) remains to be elucidated. The present study aimed to elucidate the mechanisms of MCM3AP-AS1 in the resistance of GC cells to CDDP. The expression levels of MCM3AP-AS1, miR-138 and FOXC1 were measured via reverse transcription-quantitative PCR. In addition, cell viability, migration and invasion were assessed via the Cell Counting Kit-8, wound healing and transwell assays, respectively. The interaction between genes was confirmed via the dual-luciferase reporter and pull-down assays. Western blot analysis was performed to detect FOXC1 protein expression. In the present study, it was demonstrated that MCM3AP-AS1 expression was upregulated in CDDP-resistant GC cells and that MCM3AP-AS1-knockdown suppressed CDDP resistance in GC cells. Moreover, the examination of the molecular mechanism indicated that MCM3AP-AS1 upregulated FOXC1 expression by sponging microRNA (miR)-138. Additionally, it was identified that the overexpression of FOXC1 abolished MCM3AP-AS1-knockdown- or miR-138 mimic-mediated inhibitory effects on CDDP resistance in GC cells. In conclusion, the present findings suggested that MCM3AP-AS1 enhanced CDDP resistance by sponging miR-138 to upregulate FOXC1 expression, indicating that MCM3AP-AS1 may be a novel promising biomarker for the diagnosis and treatment of patients with GC.
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