Mir-27a: A Regulator of Apaf-1, Modulate Proliferation and Apoptosis in Laryngeal Carcinoma
Received Date: Jun 07, 2016 / Accepted Date: Jun 21, 2016 / Published Date: Jun 24, 2016
Purpose: APAF-1, a key mediator in cytochrome C-dependent apoptotic pathway, plays a critical role in many cancers. MicroRNA-27a inhibits hypoxia-induced neuronal apoptosis by targeting APAF-1. Whether microRNA-27a participates in carcinogenesis via regulating APAF-1 is not reported.
Methods: Laryngeal cancer tissues, Hep2 cell line and HEK293 cell line were used in the study. qRT-PCR was used to detect microRNA-27a and APAF-1 mRNA levels. Western blot was to monitor APAF-1 protein level. Cell viability, colony formation and apoptosis assays were applied to evaluate the function of microRNA-27a and APAF-1 in laryngeal cancer. Dual-luciferase reporter assay was to detect the binding ability of microRNA-27a to APAF-1 3'UTR.
Results: In the study, we found that up-regulation of microRNA-27a was negatively correlated with downregulation of APAF-1 in laryngeal cancer. MicroRNA-27a was reconfirmed to directly bind APAF-1 mRNA 3'UTR. Similar to si-APAF-1, ectopic miR-27a significantly promoted laryngeal cancer cell proliferation and colony formation ability and suppressed early apoptosis compared to the controls.
Conclusion: miR-27a acts as a potentially oncogenic role in laryngeal squamous cell carcinoma partly though repressing APAF-1 expression, which enriches regulatory network of APAF-1 mediating apoptotic pathway.
Keywords: Laryngeal cancer; Mir-27a; Apaf-1; Proliferation; Apoptosis
Citation: Ji X, Zhang XW, Liu N, Qiu GB, Xu ZM, et al. (2016) Mir-27a: A Regulator of Apaf-1, Modulate Proliferation and Apoptosis in Laryngeal Carcinoma. Diagn Pathol Open 1: 116. Doi: 10.4172/2476-2024.1000116
Copyright: ©2016 Ji X. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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