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HOTAIRM 1 competed endogenously with miR‐148a to regulate DLGAP 1 in head and neck tumor cells
Author(s) -
Zheng Mei,
Liu Xingguang,
Zhou Qin,
Liu Gangli
Publication year - 2018
Publication title -
cancer medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 53
ISSN - 2045-7634
DOI - 10.1002/cam4.1523
Subject(s) - head and neck , microbiology and biotechnology , chemistry , biology , medicine , surgery
This study is aimed to explore the regulatory effect of lnc RNA HOTAIR /miR‐148a/ DLGAP 1 axis on head and neck tumor ( HNT ) cell growth, cell mobility, and invasiveness. HOTAIRM 1, miR‐148a, and DLGAP 1 level in HNT tissues and adjacent normal tissues were measured by qRT ‐ PCR . Cell Counting Kit‐8 ( CCK ‐8) and Transwell (migration and invasion) assay were used to survey the influence of HOTAIRM 1, miR‐148a, and DLGAP 1 on Fadu cells. Nude mouse xenograft was utilized to validate the influence of HOTAIRM 1 in vivo. Dual‐luciferase reporter assay confirms the relationship between HOTAIRM 1 and miR‐148a, miR‐148a, and DLGAP 1 . The expression level of HOTAIRM 1 was downregulated in human HNT tissues and cells. Overexpression of HOTAIRM 1 significantly moderated Fadu cells proliferation, apoptosis, migration, and invasion in vitro and impaired the tumorigenesis in vivo. The expression level of miR‐148a was upregulated in human HNT tissue compared to the adjacent tissues. We identified that miR‐148a was a target of HOTAIRM 1 and its expression levels were reduced by HOTAIRM 1. Transfection of miR‐148a mimics increased proliferation, migration, and invasion of Fadu cells. DLGAP 1 was identified as a novel target of miR‐148a and its expression level was promoted by either HOTAIRM 1 overexpression or miR‐148a knockdown. Overexpression of DLGAP 1 also facilitated the cell viability and metastasis of Fadu cells. HOTAIRM 1 was confirmed as a tumor suppressor via sponging miR‐148a and promote the expression of DLGAP 1 , which could be regarded as an important target for the prevention and treatment of HNT .

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