MiR-142 inhibits the development of cervical cancer by targeting HMGB1

Abstract

It has been reported that miRNAs is deregulated in diverse human cancers, involving human cervical cancer. However, the clinical significances and potential mechanisms of miR-142 in the development and progression of cervical cancer were not elucidated completely till now. In this study, we found that the expression of miR- 142 was obviously down-regulated in human cervical cancer tissues and a panel of cell lines. According to statistics, the expression of miR-142 was negatively related to advanced FIGO stage and lymphatic metastasis (p < 0.001). Furthermore, our functional analysis revealed the overexpression of miR-142 affected cell proliferation and invasiveness, and enhanced cell apoptosis in representative SiHa and HeLa cells. Based on the molecular level, our findings showed the 3′ untranslated region (3′-UTR) of high-mobility group box 1 protein (HMGB1) was a direct target of miR-142, and determined an inverse correlation with the expression of miR-142. Ectopic expression of HMGB1 could attenuate the inhibitory impact of miR-142 on the proliferation and invasiveness of cervical cancer cells. In conclusion, the present work suggested that miR-142 affects cervical cancer cell proliferation and invasiveness, and enhances cell apoptosis via directly targeting the expression of HMGB1, and these findings may lay a novel foundation for the promising therapy target of cervical cancer.

MicroRNA-142 Inhibits Proliferation and Promotes Apoptosis in Airway Smooth Muscle Cells During Airway Remodeling in Asthmatic Rats via the Inhibition of TGF-β -Dependent EGFR Signaling Pathway

“…Furthermore, we show that our rat asthma models exhibited reduced miR-142 expression. Relatedly, Jiang et al reported that miR-142 was expressed at low levels in several cancer tissues and was associated with pathological indicators in cancer patients; miR-142 overexpression was also found to influence prostate cancer cell growth by targeting the androgen receptor [26]. However, few studies have investigated the dynamics of miR-142 expression or the mechanism by which miR-142 exerts its effects.…”

Pathogenic role of exosomes and microRNAs in HPV‐mediated inflammation and cervical cancer: A review

“…There is a reverse association between miR‐34a, miR‐1284and miR‐142 and HMBG1 expression. Therefore, downregulation of miR‐34a, miR‐1284and miR‐142 can enhance CC proliferation, invasion and inflammation by upregulating HMGB1 . HMGB1 expression is one cause of chemoresistance, so that miR‐1284 downregulation (a tumor suppressor in CC) increases the resistance of CC cells to cisplatin and inhibits apoptosis via HMGB1 upregulation .…”

“…Therefore, downregulation of miR-34a, miR-1284and miR-142 can enhance CC proliferation, invasion and inflammation by upregulating HMGB1. [108][109][110] HMGB1 expression is one cause of chemoresistance, so that miR-1284 downregulation (a tumor suppressor in CC) increases the resistance of CC cells to cisplatin and inhibits apoptosis via HMGB1 upregulation. 109 HMGB1 plays a significant role in the lymphatic metastasis in CC patients, and it has been demonstrated that downregulation of miR-142 augments lymphatic metastasis in CC patients.…”

“…109 HMGB1 plays a significant role in the lymphatic metastasis in CC patients, and it has been demonstrated that downregulation of miR-142 augments lymphatic metastasis in CC patients. 110 Other miRNAs (miR-24, miR-451, lethal 7a [let-7a] and miR-125a) have been shown to be downregulated in CC and can induce inflammation via upregulating their target genes. The first investigation into the relationship between miRNAs and YKL-40 (also known as chitinase-3-like protein 1) in cancer was reported in 2016 by Sun et al YKL-40 is an inflammatory marker, which is targeted by miR-24.…”

Loss‐of‐function of miR‐142 by hypermethylation promotes TGF‐β‐mediated tumour growth and metastasis in hepatocellular carcinoma

“…miR‐142 was identified to dysregulated in different types of tumours. miR‐142 was up‐regulated in human breast cancer stem cells (BCSCs) as compared to the non‐tumorigenic breast cancer cells but obviously down‐regulated in human cervical cancer tissues and HCC tissues . But, to date, the courses of this dysregulation in HCC and related function have not fully understood.…”