ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016
Poly r(C) binding protein is post-transcriptionally repressed by MiR-490-3p to potentiate squamous cell carcinoma.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- MicroRNA-490-3p and -490-5p in carcinogenesis: Separate or the same goal?Oncology letters · 2021Review
- RP11-81H3.2 Acts as an Oncogene via microRNA-490-3p Inhibition and Consequential Tankyrase 2 Up-Regulation in Hepatocellular Carcinoma.Digestive diseases and sciences · 2020Article
- Integrative analysis for identification of shared markers from various functional cells/tissues for rheumatoid arthritis.Immunogenetics · 2017Article
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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
Squamous cell skin carcinoma remains a leading cause of cancer-related mortality with a huge cost of treatment, necessitating discovery and validation of potent therapeutic targets. Poly r(C) binding protein 1 (PCBP1) has been previously shown to function as a tumor suppressor. Previous work has shown that PCBP1 expression is inversely correlated to maintenance of cancer stem cells in squamous cell skin carcinoma and prostate cancer, respectively. However, the precise mechanism that regulates PCBP1 expression has not been elucidated. Here, we show that loss of PCBP1 protein expression observed in CD34+ COLO-16 cells is orchestrated by translational silencing. Translational silencing is caused by targeting of PCBP1 mRNA by miR-490-3p. Exogenous manipulation of miR-490-3p levels can accordingly modulate PCBP1 protein expression, thus suggesting that miR-490-3p as a potential biomarker in squamous cell skin cancer with therapeutic benefits.
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