ArticleThe Kaohsiung journal of medical sciences2025
PSMD14 Transcriptionally Activated by MEF2A Promotes Pancreatic Cancer Development by Upregulating SPON2 Expression.
Article in The Kaohsiung journal of medical sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Mechanism of FOXP2 in the Hepatocellular Carcinoma Progression via Ferroptosis Through RBM15B-Mediated m6A Modification.Applied biochemistry and biotechnology · 2026Article
- MEF2A activates the ZDHHC20/NF-κB pathway to inhibit doxorubicin sensitivity and promote the malignant progression of acute myeloid leukemia.Biology direct · 2026Article
- Pathological role of deubiquitinating enzymes in lung cancer: recent insights and advances.American journal of cancer research · 2026Review
- Role of human Myocyte Enhancer Factor 2 (MEF2) proteins in cancer: structural insights, functional diversity, and regulatory mechanisms.Cancer cell international · 2025Review
- Role, mechanism, and application of N6-methyladenosine in hepatobiliary carcinoma.World journal of gastrointestinal oncology · 2025Review
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Authors and funding
4 authors.
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Abstract
Proteasome 26S subunit non-ATPase 14 (PSMD14) plays a pro-carcinogenic role in various cancers. However, its specific effects and mechanisms in pancreatic cancer (PC) remain unclear. We aimed to assess the function and mechanism of PSMD14 in PC. Fifteen paired pancreatic ductal adenocarcinoma (PDAC) tissues and adjacent non-tumorous tissues were clinically obtained. Cell proliferation, migration, and invasion were assessed using colony formation, scratch, and Transwell assays. The interaction between the MEF2A transcription factor and the PSMD14 promoter verified by chromatin immunoprecipitation (ChIP) or dual luciferase assay. The interaction between RBM15B and SPON2 mRNA was validated by RNA immunoprecipitation (RIP) assay. The interaction between the proteins PSMD14 and RBM15B was detected by co-immunoprecipitation (Co-IP) assay. The m6A level of SPON2 was detected by methylated RNA immunoprecipitation (MeRIP, a common method for detecting m6A levels of mRNAs). The ubiquitination level of RNA-binding motif protein 15B (RBM15B) was detected using Co-IP. The role of PSMD14 in PC was further explored subcutaneous and lung metastasis models. PSMD14 was upregulated in PDAC tissues. PSMD14 knockdown inhibited PC cell viability, proliferation, migration, and invasion. MEF2A transcriptionally activated PSMD14 expression. PSMD14 knockdown promoted the ubiquitination degradation of RBM15B. Additionally, PSMD14 enhanced SPON2 mRNA stability through RBM15B-mediated m6A modification. SPON2 overexpression impaired the effect of knockdown PSMD14. Finally, PSMD14 knockdown in PC arrested tumor growth and lung metastasis. PSMD14, transcriptionally activated by MEF2A, promotes the de-ubiquitination of RBM15B, which upregulates SPON2 expression in an m6A-RBM15B-dependent manner, thereby facilitating PC proliferation, migration, and invasion.
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