ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016
miR-16 induction after CDK4 knockdown is mediated by c-Myc suppression and inhibits cell growth as well as sensitizes nasopharyngeal carcinoma cells to chemotherapy.
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 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- A review on the role of cyclin dependent kinases in cancers.Cancer cell international · 2022Review
- The Role of Non-Coding RNAs in Controlling Cell Cycle Related Proteins in Cancer Cells.Frontiers in oncology · 2020Review
- Co-Expression Network Analysis Identifies miRNA⁻mRNA Networks Potentially Regulating Milk Traits and Blood Metabolites.International journal of molecular sciences · 2018Article
- Long non-coding RNA PVT1 predicts poor prognosis and induces radioresistance by regulating DNA repair and cell apoptosis in nasopharyngeal carcinoma.Cell death & disease · 2018Article
- Pien Tze Huang inhibits the growth of hepatocellular carcinoma cells by upregulating miR-16 expression.Oncology letters · 2017Article
- Interactions between anticancer active platinum complexes and non-coding RNAs/microRNAs.Non-coding RNA research · 2017Review
- Jungermannenone A and B induce ROS- and cell cycle-dependent apoptosis in prostate cancer cells in vitro.Acta pharmacologica Sinica · 2016Article
- MicroRNA-based screens for synthetic lethal interactions with c-Myc.RNA & disease (Houston, Tex.) · 2016Article
- Identification of key genes involved in nasopharyngeal carcinoma.Brazilian journal of otorhinolaryngologyArticle
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cyclin-dependent kinase 4 (CDK4) is a member of cyclin-dependent kinase family which regulates G1 to S cell cycle transition. CDK4 activity is increased in many tumor types. Here, we report a negative automodulatory feedback loop between CDK4 and miR-16 that regulates cell cycle progression in nasopharyngeal carcinoma (NPC). By miRNA array and real-time PCR, we identified upregulation of tumor suppressor miR-16a, which inhibited cell cycle progression and sensitized NPC cells to chemotherapy. CDK4 knockdown reduced the expression of c-Myc, the latter of which directly suppresses the miR-16 expression by directly binding to the miR-16 promoter. Moreover, we found that miR-16 upregulation could reduce CDK4 expression by repressing CCND1 and thus forms a feedback loop via the CDK4/c-Myc/miR-16/CCND1 pathway. Finally, miR-16 was negatively correlated with CDK4 expression in NPC biopsies. In summary, our results define a double-negative feedback loop involving CDK4 and miR-16 mediated by c-Myc that modulates NPC cell growth and chemotherapy sensitivity.
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Registered trials
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