ArticleCell death & disease2022
MEX3A promotes the malignant progression of ovarian cancer by regulating intron retention in TIMELESS.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- Comprehensive pan-cancer analysis of MEX3A in human tumors.Discover oncology · 2026Article
- Long non-coding RNA KCNQ1OT1 promotes ovarian cancer cell malignant characteristics by targeting the miR-140-5p/KLK10 axis.Experimental and therapeutic medicine · 2026Article
- A novel function of STARD7: its tumor-promoting role involves the activation of NF-κB signaling pathway in ovarian cancer.Human cell · 2025Article
- MEX3A: A promising prognostic marker and therapeutic target in hepatocellular carcinoma.World journal of gastrointestinal oncology · 2025Article
- Role of MEX3A in tumorigenesis: Mechanisms, tumor‑specific effects and therapeutic implications (Review).International journal of molecular medicine · 2025Review
- SNRPB-mediated regulation of DDX39A splicing promotes ovarian cancer progression by regulating α6 integrin subunit expression.Oncogene · 2025Article
- Comprehensive bioinformatics analysis of MEX3 family genes in hepatocellular carcinoma.Scientific reports · 2025Article
- MEX3A promotes cell proliferation by regulating the RORA/β-catenin pathway in hepatocellular carcinoma.World journal of gastrointestinal oncology · 2025Article
- MEX3A is a diagnostic, independent prognostic biomarker and a promising therapeutic target in glioblastoma.Frontiers in oncology · 2025Article
- Highly Efficient Synergistic Chemotherapy and Magnetic Resonance Imaging for Targeted Ovarian Cancer Therapy Using Hyaluronic Acid-Coated Coordination Polymer Nanoparticles.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Alternative splicing in ovarian cancer.Cell communication and signaling : CCS · 2024Review
- From clinical management to personalized medicine: novel therapeutic approaches for ovarian clear cell cancer.Journal of ovarian research · 2024Review
- SH3RF2 contributes to cisplatin resistance in ovarian cancer cells by promoting RBPMS degradation.Communications biology · 2024Article
- Mex3a promoter hypomethylation can be utilized to diagnose HBV-associated hepatocellular carcinoma: a randomized controlled trial.Frontiers in pharmacology · 2024Article
- Review
- MEX3A Mediates p53 Degradation to Suppress Ferroptosis and Facilitate Ovarian Cancer Tumorigenesis.Cancer research · 2023Article
- Comprehensively analyzing the genetic alterations, and identifying key genes in ovarian cancer.Oncology research · 2023Article
- Comprehensive Analysis of METTLs (METTL1/13/18/21A/23/25/2A/2B/5/6/9) and Associated mRNA Risk Signature in Hepatocellular Carcinoma.Analytical cellular pathology (Amsterdam) · 2023Article
- RNA-Binding Protein MEX3A Interacting with DVL3 Stabilizes Wnt/β-Catenin Signaling in Endometrial Carcinoma.International journal of molecular sciences · 2022Article
- HNRNPU promotes the progression of triple-negative breast cancer via RNA transcription and alternative splicing mechanisms.Cell death & disease · 2022Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The latest research shows that RNA-binding proteins (RBPs) could serve as novel potential targets for cancer therapy. We used bioinformatics analysis to screen and identify the key RBPs in ovarian cancer, from which we found that Mex-3 RNA Binding Family Member A (MEX3A) was intimately associated with the clinical prognosis of ovarian cancer. Nevertheless, little is known about its biological roles in ovarian cancer. In this case, we observed that MEX3A was highly overexpressed in fresh-frozen ovarian cancer tissues. MEX3A knockdown suppressed the development and invasion of ovarian cancer cells, while MEX3A overexpression promoted the proliferation and invasion of ovarian cancer cells. Mechanistically, TIMELESS was the critical downstream target gene of MEX3A, as demonstrated through alternative splicing event analysis based on RNA-seq. MEX3A knockdown resulted in retention of intron twenty-three of TIMELESS mRNA and decreased TIMELESS mRNA owing to stimulation of nonsense-mediated RNA decay (NMD). Additionally, we found that TIMELESS overexpression with MEX3A knockdown partially restored the proliferation ability of ovarian cancer cells. The results of this paper demonstrated that the MEX3A/TIMELESS signaling pathway was a key regulator of ovarian cancer, and MEX3A was a novel possible treatment target for ovarian cancer patients.
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