piR‐823 contributes to colorectal tumorigenesis by enhancing the transcriptional activity of HSF1
| Autor: | Jie Yin, Huiqing Jiang, Yun Bai, Dong-xuan Zhang, Jia Wang, Zi-Jin Cui, Chenguang Ji, Cunkai Wang, Xiao-Li Xie, Xiaoyu Jiang, Wei Qi |
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| Jazyk: | angličtina |
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Male Transcriptional Activation Cancer Research Transcription Genetic Somatic cell Carcinogenesis heat shock protein colorectal cancer Apoptosis piRNA Biology medicine.disease_cause 03 medical and health sciences Heat Shock Transcription Factors Heat shock protein medicine Humans Phosphorylation RNA Small Interfering HSF1 Transcription factor Cell Proliferation Cell growth General Medicine Original Articles Cell cycle Middle Aged HCT116 Cells Up-Regulation DNA-Binding Proteins Gene Expression Regulation Neoplastic 030104 developmental biology heat shock factor 1 Cell Transformation Neoplastic Oncology Cell culture Cancer research non‐coding RNAs Original Article Female Colorectal Neoplasms Protein Processing Post-Translational Protein Binding Transcription Factors |
| Zdroj: | Cancer Science |
| ISSN: | 1349-7006 1347-9032 |
| Popis: | Piwi-interacting RNAs (piRNAs), a novel class of small non-coding RNAs, were first discovered in germline cells and are thought to silence transposons in spermatogenesis. Recently, piRNAs have also been identified in somatic tissues, and aberrant expression of piRNAs 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 HCT116 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 HSPs 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 HSF1, the common transcription factor of HSPs, by binding to HSF1 and promoting its phosphorylation at Ser326. Our study reveals that piR-823 plays a tumor-promoting role by upregulating phosphorylation and transcriptional activity of HSF1 and suggests piR-823 as a potential therapeutic target for CRC. |
| Databáze: | OpenAIRE |
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