
LncRNA FAM83H‐AS1 promotes oesophageal squamous cell carcinoma progression via miR‐10a‐5p/Girdin axis
Author(s) -
Feng Bo,
Wang Gaoyan,
Liang Xiaoliang,
Wu Zheng,
Wang Xinchen,
Dong Zhiming,
Guo Yanli,
Shen Supeng,
Liang Jia,
Guo Wei
Publication year - 2020
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.15530
Subject(s) - biology , competing endogenous rna , cancer research , epithelial–mesenchymal transition , biomarker , microrna , long non coding rna , cell , antisense rna , cancer , metastasis , messenger rna , downregulation and upregulation , gene , biochemistry , genetics
Long non‐coding RNAs (lncRNAs) have been well demonstrated to emerge as crucial regulators in cancer progression, and they can function as regulatory network based on their interactions. Although the biological functions of FAM83H‐AS1 have been confirmed in various tumour progressions, the underlying molecular mechanisms of FAM83H‐AS1 in oesophageal squamous cell carcinoma (ESCC) remained poorly understood. To address this, we treated human oesophageal cancer cell line Eca109 cells with TGF‐β and found FAM83H‐AS1 was notably overexpressed. In the present study, FAM83H‐AS1 was observed to be significantly up‐regulated in ESCC tissues and was associated with TNM stage, pathological differentiation and lymph node metastasis. FAM83H‐AS1 reinforced oesophageal cancer cell proliferation, migration and invasion, and participated in epithelial‐to‐mesenchymal transition (EMT) process at mRNA and protein levels. In addition, a concordant regulation between FAM83H‐AS1 and its sense strand FAM83H was detected at the transcriptional and translational levels. Furthermore, FAM83H‐AS1 could act as competing endogenous RNA to affect the expression of Girdin by sponging miR‐10a‐5p verified by RIP and luciferase reporter assays. Consequently, the study provided a unique perspective of FAM83H‐AS1 in ESCC progression, which may be considered as potential biomarker and therapeutic target for ESCC therapy.