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Long noncoding RNA lnc‐ABCA12‐3 promotes cell migration, invasion, and proliferation by regulating fibronectin 1 in esophageal squamous cell carcinoma
Author(s) -
Ma Junliang,
Xiao Yuhang,
Tian Bo,
Chen Shaolin,
Zhang Baihua,
Wu Jie,
Wu Zhining,
Li Xu,
Tang Jinming,
Yang Desong,
Zhou Yong,
Wang Hui,
Su Min,
Wang Wenxiang
Publication year - 2020
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.29373
Subject(s) - downregulation and upregulation , long non coding rna , cancer research , gene knockdown , biology , cell migration , cell growth , carcinogenesis , fibronectin , oncogene , competing endogenous rna , cell , microbiology and biotechnology , apoptosis , cancer , cell cycle , gene , biochemistry , genetics
Long noncoding RNAs (lncRNAs) have been shown to play important roles in human cancers, including esophageal squamous cell carcinoma (ESCC). We previously demonstrated that a novel lncRNA, lnc‐ABCA12‐3, was overexpressed in ESCC tissues. However, the exact function of lnc‐ABCA12‐3 is unknown. In the current study, we aimed to evaluate the expression of lnc‐ABCA12‐3 in ESCC and to explore the potential mechanism of lnc‐ABCA12‐3 in cell migration, invasion, and proliferation. We showed that lnc‐ABCA12‐3 was upregulated in ESCC tumor tissues and cell lines. The increased expression of lnc‐ABCA12‐3 was positively associated with advanced tumor‐node‐metastasis stages and poor prognosis. The knockdown of lnc‐ABCA12‐3 inhibited the cell migration, invasion, and proliferation abilities of KYSE‐510 and Eca‐109 cells. We also found that fibronectin 1 (FN1) was upregulated in ESCC tumor tissues. The expression of FN1 messenger RNA was positively correlated with the expression of lnc‐ABCA12‐3 in ESCC tumor tissues. After lnc‐ABCA12‐3 knockdown, the expression of FN1 was downregulated. In addition, the overexpression of FN1 restored the abilities of cell migration, invasion and proliferation in Eca‐109 cells. Further studies indicated that lnc‐ABCA12‐3 acted as a competing endogenous RNA for miR‐200b‐3p to regulate FN1 expression. In conclusion, these results suggest that lnc‐ABCA12‐3 is a novel oncogene in tumorigenesis and that its high expression is related to a poor prognosis for patients with ESCC. lnc‐ABCA12‐3 promotes cell migration, invasion, and proliferation via the regulation of FN1 in ESCC. Our data suggest that lnc‐ABCA12‐3 might serve as a potential prognostic biomarker and therapeutic target for ESCC.