MicroRNA‐22 suppresses cell proliferation, migration and invasion in oral squamous cell carcinoma by targeting NLRP3

MicroRNAs (miRNAs) have been implicated as important regulators of carcinogenesis and tumor development. Recently, microRNA‐22 (miR‐22) has been reported to be a cancer‐related miRNA in several types of tumors. In this study, we aimed to investigate the role of miR‐22 in oral squamous cell carcinoma...

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Veröffentlicht in:Journal of cellular physiology 2018-09, Vol.233 (9), p.6705-6713
Hauptverfasser: Feng, Xiaodong, Luo, Qingqiong, Wang, Han, Zhang, Han, Chen, Fuxiang
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Sprache:eng
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Zusammenfassung:MicroRNAs (miRNAs) have been implicated as important regulators of carcinogenesis and tumor development. Recently, microRNA‐22 (miR‐22) has been reported to be a cancer‐related miRNA in several types of tumors. In this study, we aimed to investigate the role of miR‐22 in oral squamous cell carcinoma (OSCC). We found that miR‐22 expression was significantly decreased in OSCC tissues compared with that in the adjacent noncancerous tissues. Furthermore, lentivirus‐mediated miR‐22 overexpression markedly reduced OSCC cell viability, migration and invasion, whereas miR‐22 inhibitor promoted these parameters. Mechanistically, NLR family pyrin domain containing three (NLRP3) was identified as a direct target of miR‐22. miR‐22 expression was inversely correlated with NLRP3 expression both in OSCC tissues and cell lines. Moreover, overexpression of miR‐22 in OSCC cells could reverse the tumor‐promoting effect of the activated NLRP3 inflammasome and vice versus. Therefore, our results indicate that miR‐22 may play a suppressive role in OSCC by targeting NLRP3, which offer new insights into the molecular mechanisms of the growth and metastasis of OSCC. miR‐22 expression was significantly decreased in OSCC tissues compared with that in the adjacent noncancerous tissues. NLR family pyrin domain containing 3 (NLRP3) was identified as a direct target of miR‐22. Overexpression of miR‐22 in OSCC cells could reverse the tumor‐promoting effect of the activated NLRP3 inflammasome and vice versus.
ISSN:0021-9541
1097-4652
DOI:10.1002/jcp.26331