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HOXC13‐AS promotes breast cancer cell growth through regulating miR‐497‐5p/PTEN axis
Author(s) -
Li Xiaowei,
Wang Qiang,
Rui Yiqi,
Zhang Chuanqiang,
Wang Wenwen,
Gu Jianchun,
Tang Jinhai,
Ding Yongbin
Publication year - 2019
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.28800
Subject(s) - pten , tensin , cancer research , carcinogenesis , downregulation and upregulation , cell growth , oncogene , biology , breast cancer , competing endogenous rna , cancer , cell , long non coding rna , signal transduction , pi3k/akt/mtor pathway , microbiology and biotechnology , cell cycle , gene , genetics
Abstract Dysregulated long noncoding RNAs (lncRNAs) remains to be explored in tumorigenesis. LncRNA HOXC13 antisense RNA (HOXC13‐AS) has been found as an oncogene in many cancers; however, the role of HOXC13‐AS in breast cancer still elusive. In this study, the HOXC13‐AS levels and its role in cell proliferation was first measured by real‐time quantitative polymerase chain reaction, Cell Counting Kit‐8 assay, and colony formation assay. It showed that HOXC13‐AS was increased in breast cancer tissues compared with the adjacent normal tissues and upregulated HOXC13‐AS promoted the growth of breast cancer cells. Then, we found that the miR‐497‐5p levels were downregulated in cancer tissues compared with the adjacent tissues and miR‐497‐5p suppressed breast cancer cell proliferation. Further study showed that HOXC13‐AS could function as a “sponge” for miR‐497‐5p then suppress miR‐497‐5p expression. Moreover, we next identified that Phosphatase and Tensin homolog (PTEN) is the target of miR‐497‐5p. Overexpression of miR‐497‐5p by chemical mimics decreased the expression of PTEN, while downregulation of miR‐497‐5p by HOXC13‐AS rescued the expression of PTEN. Finally, we showed that HOXC13‐AS promoted the proliferation of breast cancer cells and tumor growth through miR‐497‐5p/PTEN axis in vitro and in vivo. Hence, we conclude that HOXC13‐AS, which is significantly upregulated in breast cancers, promoted cell proliferation through the suppressed miR‐497‐5p and further upregulated PTEN.