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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 χ2 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.
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Song et al. (2017) studied this question.
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