ArticleThe Kaohsiung journal of medical sciences2021
S100P acts as a target of miR-495 in pancreatic cancer through bioinformatics analysis and experimental verification.
Article in The Kaohsiung journal of medical sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 5 citations in OpenAlex.
- Abnormal levels of miRNA in pancreatic cancer are linked to tumor progression by regulating the translation of tumor-associated mRNA.Annals of medicine · 2025Review
- Multiple roles of S100P in pan carcinoma: Biological functions and mechanisms (Review).Oncology reports · 2025Review
- MicroRNA-495: a therapeutic and diagnostic tumor marker.Journal of molecular histology · 2023Review
- Screening of Therapeutic Targets for Pancreatic Cancer by Bioinformatics Methods.Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme · 2023Article
- The Interaction Between Non-Coding RNAs and Calcium Binding Proteins.Frontiers in oncology · 2022Review
- S100P acts as a target of miR-495 in pancreatic cancer through bioinformatics analysis and experimental verification.The Kaohsiung journal of medical sciences · 2021Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
S100 calcium binding protein P (S100P) and miR-495 are aberrantly expressed and exert essential roles in cancers. However, the mechanisms of miR-495-S100P in pancreatic cancer are yet to be illustrated. Thus, we explored the regulatory functions of miR-495-S100P axis in pancreatic adenocarcinoma cells growth and invasion. In this study, we identified that S100P was upregulated in pancreatic adenocarcinoma by bioinformatics analysis of the GEO (Gene Expression Omnibus database) microarray dataset (GSE16515). Western blotting and luciferase reporter gene analysis exhibited that miR-495 negatively determined the level of S100P via binging to its 3'-untranslated regions (3'-UTRs). A series of functional experiments indicated that upregulation of miR-495 or S100P knockdown suppressed pancreatic adenocarcinoma cells proliferation, invasion, and promoted apoptosis. Furthermore, the expression of S100P was negatively associated with the level of miR-495 in The Cancer Genome Atlas (TCGA) pancreatic adenocarcinoma case-cohort. Besides, reintroduction of S100P debilitated the anti-cancer action of miR-495 in pancreatic adenocarcinoma cells. Our data indicated that miR-495 performed suppressive roles in pancreatic adenocarcinoma through targeting S100P.
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Registered trials
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.