Open AccessLncRNA NEAT1 promotes cell proliferation, migration, and invasion via the miR ‐186‐5p/ PTP4A1 axis in cholangiocarcinoma
Author(s) -
Li Ou,
Jiang Bo,
Yi WeiMin,
Zhang Yu,
Yang PinZhou,
Guo Chao,
Sun ZengPeng,
Peng Chuang
Publication year - 2021
Publication title -
the kaohsiung journal of medical sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.439
H-Index - 36
eISSN - 2410-8650
pISSN - 1607-551X
DOI - 10.1002/kjm2.12354
Subject(s) - gene knockdown , downregulation and upregulation , protein kinase b , cell growth , flow cytometry , pi3k/akt/mtor pathway , microrna , cancer research , epithelial–mesenchymal transition , apoptosis , gentamicin protection assay , cell migration , cell , medicine , microbiology and biotechnology , metastasis , signal transduction , biology , cancer , gene , biochemistry
Cholangiocarcinoma (CCA) is a highly aggressive and malignant tumor. In this study, the effect and molecular mechanism of nuclear enriched abundant transcript 1 (NEAT1) in CCA were elucidated. The expressions of NEAT1, microRNA‐186‐5p (miR‐186‐5p), and PTP4A1 were measured by quantitative real‐time PCR. The protein levels were measured by Western blotting. Kaplan–Meier analysis was performed to create survival curves. The interactions between NEAT1, miR‐186‐5p, and PTP4A1 were assessed through the dual luciferase reporter assay. Additionally, the cell proliferation, apoptosis, migration, and invasion were measured by colony formation, flow cytometry, the Transwell assay, and the wound healing assay, respectively. NEAT1 and PTP4A1 were significantly upregulated in CCA tissues and cells, but miR‐186‐5p was downregulated. NEAT1 expression was negatively correlated with the survival of CCA patients and has remarkable correlation with serum CA199 levels and lymph node metastasis. Besides, NEAT1 could act as a molecular sponge for miR‐186‐5p to upregulate PTP4A1 expression. More importantly, the knockdown of NEAT1 or overexpression of miR‐186‐5p inhibited the proliferation, migration and invasion of CCA cells, and the inhibition of miR‐186‐5p reversed the effects of the knockdown of NEAT1. In addition, NEAT1 could also activate the PI3K/AKT signaling pathway and regulate the epithelial‐mesenchymal transition (EMT) through the miR‐186‐5p/PTP4A1 axis. In conclusion, NEAT1 was involved in cell proliferation, migration and invasion in CCA, and the NEAT1/miR‐186‐5p/PTP4A1/PI3K/AKT axis indicated novel regulatory mechanisms and therapeutics for the treatment of CCA.