HLA-F-AS1/miR-330-3p/PFN1 axis promotes colorectal cancer progression

Accumulating Studies implies that long-chain non-coding RNA (lncRNA) plays a vital regulatory role in the occurrence and progression of tumors. This study aimed to explore the function and mechanism of lncRNA HLA-F antisense RNA 1 (HLA-F-AS1) in colorectal cancer (CRC). Expressions of HLA-F-AS1, miR...

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Veröffentlicht in:Life sciences (1973) 2020-08, Vol.254, p.117180-9, Article 117180
Hauptverfasser: Huang, Yongguo, Sun, Hong, Ma, Xiang, Zeng, Ye, Pan, Yang, Yu, Dongyang, Liu, Zhisheng, Xiang, Yun
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Sprache:eng
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Zusammenfassung:Accumulating Studies implies that long-chain non-coding RNA (lncRNA) plays a vital regulatory role in the occurrence and progression of tumors. This study aimed to explore the function and mechanism of lncRNA HLA-F antisense RNA 1 (HLA-F-AS1) in colorectal cancer (CRC). Expressions of HLA-F-AS1, miR-330-3p and profilin 1 (PFN1) mRNA in CRC tissues were detected by RT-PCR. MTT assay was used to detect cell proliferation, and Transwell assay was used to detect cell migration and invasion. In addition, PFN1 and apoptosis-related protein Bcl-2 associated X (Bax) and B cell lymphoma/leukmia-2 (Bcl2) were detected by western blot. Interactions between miR-330-3p and HLA-F-AS1 or the 3′UTR of PFN1 were predicted and determined by bioinformatics analysis and luciferase reporter assay. Expressions of HLA-F-AS1 and PFN1 were significantly up-regulated while miR-330-3p was significantly down-regulated in CRC tissues and cell lines. Over-expressions of HLA-F-AS1 or transfection of miR-330-3p inhibitors could promote the proliferation, migration and invasion and block apoptosis of CRC cells, whereas knockdown of HLA-F-AS1 or transfection of miR-330-3p mimics led to the opposite effects. Additionally, HLA-F-AS1 could down-regulate miR-330-3p via sponging it. HLA-F-AS1 also enhanced the expressions of PFN1, which was validated as a target gene of miR-330-3p. HLA-F-AS1 promoted CRC progression via regulating miR-330-3p/PFN1 axis.
ISSN:0024-3205
1879-0631
DOI:10.1016/j.lfs.2019.117180