piR‐823 contributes to colorectal tumorigenesis by enhancing the transcriptional activity of HSF1

Piwi‐interacting RNA s (pi RNA s), a novel class of small non‐coding RNA s, were first discovered in germline cells and are thought to silence transposons in spermatogenesis. Recently, pi RNA s have also been identified in somatic tissues, and aberrant expression of pi RNA s in tumor tissues may be implicated in carcinogenesis. However, the function of piR‐823 in colorectal cancer ( CRC ) remains unclear. Here, we first found that piR‐823 was significantly upregulated in CRC tissues compared with its expression in the adjacent tissues. Inhibition of piR‐823 suppressed cell proliferation, arrested the cell cycle in the G1 phase and induced cell apoptosis in CRC cell lines HCT 116 and DLD ‐1, whereas overexpression of piR‐823 promoted cell proliferation in normal colonic epithelial cell line FHC . Interestingly, Inhibition of piR‐823 repressed the expression of heat shock protein ( HSP ) 27, 60, 70. Furthermore, elevated HSP s expression partially abolished the effect of piR‐823 on cell proliferation and apoptosis. In addition, we further demonstrated that piR‐823 increased the transcriptional activity of HSF 1, the common transcription factor of HSP s, by binding to HSF 1 and promoting its phosphorylation at Ser326. Our study reveals that piR‐823 plays a tumor‐promoting role by upregulating phosphorylation and transcriptional activity of HSF 1 and suggests piR‐823 as a potential therapeutic target for CRC .