ArticleBMC cancer2014
Knocking down CDK4 mediates the elevation of let-7c suppressing cell growth in nasopharyngeal carcinoma.
Article in BMC cancer, 2014. 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, 44 citations in OpenAlex.
- Dysregulated miRNA Expression and Its Association with Immune Checkpoints in Head and Neck Cancer.Cancers · 2025Article
- Identification and Analysis of Immune-Related Gene Signature in Hepatocellular Carcinoma.Genes · 2022Article
- Curcumin Sensitises Cancerous Kidney Cells to TRAIL Induced Apoptosis via Let-7C Mediated Deregulation of Cell Cycle Proteins and Cellular Metabolism.International journal of molecular sciences · 2022Article
- Hedyotis diffusae Herba-Andrographis Herba inhibits the cellular proliferation of nasopharyngeal carcinoma and triggers DNA damage through activation of p53 and p21.Cancer gene therapy · 2022Article
- CDK6-PI3K signaling axis is an efficient target for attenuating ABCB1/P-gp mediated multi-drug resistance (MDR) in cancer cells.Molecular cancer · 2022Article
- Ribociclib Inhibits P-gp-Mediated Multidrug Resistance in Human Epidermoid Carcinoma Cells.Frontiers in pharmacology · 2022Article
- Investigation of differentially expressed genes in nasopharyngeal carcinoma by integrated bioinformatics analysis.Oncology letters · 2019Article
- Effects of SIRT1 silencing on viability, invasion and metastasis of human glioma cell lines.Oncology letters · 2019Article
- MicroRNA-92a Promotes Cell Proliferation in Cervical Cancer via Inhibiting p21 Expression and Promoting Cell Cycle Progression.Oncology research · 2017Article
- Mouse models of Down syndrome: gene content and consequences.Mammalian genome : official journal of the International Mammalian Genome Society · 2016Review
- MicroRNA-98 acts as a tumor suppressor in hepatocellular carcinoma via targeting SALL4.Oncotarget · 2016Article
- Article
- The putative tumor activator ARHGEF3 promotes nasopharyngeal carcinoma cell pathogenesis by inhibiting cellular apoptosis.Oncotarget · 2016Article
- Article
- 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.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Suppressive Role of MicroRNA-148a in Cell Proliferation and Invasion in Ovarian Cancer Through Targeting Transforming Growth Factor-β-Induced 2.Oncology research · 2016Article
- MicroRNA-200b acts as a tumor suppressor in osteosarcoma via targeting ZEB1.OncoTargets and therapy · 2016Article
- Genomic insights into head and neck cancer.Cancers of the head & neck · 2016Article
- Let-7a inhibits migration, invasion and epithelial-mesenchymal transition by targeting HMGA2 in nasopharyngeal carcinoma.Journal of translational medicine · 2015Article
- Elevated nuclear CCND1 expression confers an unfavorable prognosis for early stage lung adenocarcinoma patients.International journal of clinical and experimental pathology · 2015Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCDK4 is a protein kinase in the CDK family important for G1/S phase cell cycle progression. However, the roles and molecular mechanisms of CDK4 triggering nasopharynx carcinogenesis are still unclear.
methodsLentiviral-vector mediated shRNA was used to suppress CDK4 expression and examine its molecular mechanisms. Using immunohistochemistry, we analyzed CDK4 protein expression in clinicopathologically characterized nasopharyngeal carcinoma (NPC) cases and nasopharyngeal tissues (NPs). Survival curves were plotted by the Kaplan-Meier method and compared using the log-rank test.
resultsIn this investigation, we knocked down CDK4 expression and observed that NPC cell growth and cell cycle progression were significantly blocked by suppressing expression of CCND1, CDK6, and E2F1 as well as elevated p21 expression. Further, we found that reduced CDK4 expression elevated the expression of let-7c, a tumor-suppressive miRNA modulated by E2F1. We found that let-7c was markedly downregulated in NPC tissues compared to NPs and suppressed cell growth and cell cycle progression by modulating p15/p16/CDK4/E2F1 pathway. Finally, CDK4 protein was observed to be overexpressed in NPC tissues and could be considered an unfavorable prognosis factor for NPC patients although its independent prognostic value did not reach statistical significance (p = 0.087).
conclusionsOur results demonstrated that overexpressed CDK4 is an unfavorable prognostic factor which suppresses the expression of tumor suppressive-factor let-7c through p21/CCND1/CDK6/E2F1 signaling, and inhibits cell proliferation by p15/p16/CDK4/E2F1 feedback signaling in NPC.
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