Open AccesslncRNA FAM83H‑AS1 is associated with the prognosis of colorectal carcinoma and promotes cell proliferation by targeting the Notch signaling pathway
Author(s) -
Lingyun Song,
Wei Dong,
Pei Zhao,
Zhenjun Liu
Publication year - 2017
Publication title -
oncology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.766
H-Index - 54
eISSN - 1792-1082
pISSN - 1792-1074
DOI - 10.3892/ol.2017.7520
Subject(s) - oncogene , cell cycle , cancer research , notch signaling pathway , colorectal cancer , cell growth , molecular medicine , cell , apoptosis , signal transduction , biology , medicine , oncology , cancer , microbiology and biotechnology , genetics
The long non-coding RNA, FAM83H antisense RNA 1 (head to head) (FAM83H-AS1), has exhibited a functional role as an oncogene in a number of different types of cancer. The aim of the present study was to reveal the dysregulation of FAM83H-AS1 in colorectal carcinoma (CRC) samples and elucidate its underlying associations with the Notch signaling pathway. The expression profiles of FAM83H-AS1 and two Notch signaling-associated molecules, Notch1 and Hes family basic-helix-loop-helix transcription factor 1 (Hes1), were measured by reverse transcription-polymerase chain reaction and western blot analysis. The Pearson χ 2 test was employed to evaluate the associations between FAM83H-AS1 expression and clinical features. A statistically significant positive association between the expression levels of FAM83H-AS1 and those of Notch1 or Hes1 in CRC tissues was analyzed by Spearman's correlation analysis. The Kaplan-Meier method was used to compare the overall survival curves between the highly-expressed and low-expressed FAM83H-AS1 groups via a log-rank test. Specific small hairpin RNA was transfected to silence endogenous FAM83H-AS1. MTT and colony formation assays were performed to measure the growth-inhibition effect of silenced FAM83H-AS1. The levels of FAM83H-AS1, Notch1 and Hes1 were significantly increased in CRC samples and cell lines. Cell proliferation was markedly inhibited when FAM83H-AS1 was knocked down and this effect mediated by FAM83H-AS1 could be reversed by Notch1 regulators. Thus, downregulated FAM83H-AS1 exhibited an anti-proliferative role in CRC by repressing the Notch signaling pathway.