MiRNA-106a-5p Promotes Laryngeal Carcinoma Proliferation and Migration Through PI3K/AKT/m-TOR Pathway by AKTIP

Document Type : Research Paper


1 Department of Rheumatology and Immunology, First Affiliated Hospital of Jinzhou Medical University. Jinzhou City, Liaoning Province, China

2 Department of Otolaryngology, First Affiliated Hospital of Jinzhou Medical University. Jinzhou City, Liaoning Province, China



Background: Laryngeal cancer (LC) remains one of the most common tumors of the respiratory tract, the exact pathogenesis remains unclear. MiRNA-106a-5p is aberrantly expressed in a variety of cancers and plays a pro- or anti-cancer role, but is indistinct in LC.
Objectives: Showing the role of miRNA-106a-5p in the development of LC.
Materials and Methods: Quantitative reverse transcription-polymerase chain reaction was used for miR-106a-5p measurement in clinical samples and LC cell lines (AMC-HN8 and TU212), first. The expression of miR-106a-5p was inhibited by inhibitor, then followed clonogenic and flow cytometric assays for cell proliferation; wood healing, and Transwell assays for cell migration. Dual luciferase reporter assay was performed for interaction verification, and the activation of the signal pathway was detected by western blots.
Results: MiR-106a-5p was significantly over-expressed in LC tissues and cell lines. The proliferation ability of the LC cells was significantly reduced after miR-106a-5p inhibition, and most LC cells were stagnated in the G1 phase. The migration and invasion ability of the LC cells was decreased after the miR-106a-5p knockdown. Further, we found that miR-106-5a is bound with 3’-UTR of AKT interacting protein (AKTIP) mRNA specifically, and then activate PI3K/AKT/m-TOR pathway in LC cells.
Conclusions: A new mechanism was uncovered that miR-106a-5p promotes LC development via AKTIP/PI3K/AKT/m-TOR axis, which guides clinical management and drug discovery.


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