Abstract
Increasing evidence has demonstrated that miRNAs play a critical role in tumor development and progression. Previous studies have revealed that miR-106a is abnormally expressed in various cancers. However, its function and underlying mechanism in cervical cancer (CC) remains unknown. In this study, we confirmed that the expression of miR-106a was significantly upregulated in both CC cell lines and tissues by qRT-PCR. The increased expression of miR-106a was obviously associated with adverse prognostic features. Moreover, we demonstrated that miR-106a was a novel independent prognostic marker for predicting the 5-year survival of CC patients. The ectopic overexpression of miR‑106a promoted cell migration, invasion and invasion-related gene expression, while downregulated miR-106a reversed the effect. In addition, miR-106a regulated tissue inhibitor of metalloproteinase (TIMP)2 by directly binding to its 3'-UTR, leading to the indution of the expression of matrix metalloproteinases (MMPs). In clinical samples of CC, miR-106a was inversely correlated with TIMP2, which was downregulated in CC. Alteration of TIMP2 expression at least partially abolished the migration, invasion and MMP expression of miR-106a in CC cells. In conclusion, our data indicated that miR-106a promoted the migration, invasion and MMP expression of CC by targeting TIMP2, and may represent a novel potential therapeutic target and prognostic marker for CC.
Highlights
Cervical cancer (CC) is one of the most common cancers and the third leading cause of cancer-related deaths in womenKey words: microRNA-106a, cervical cancer, TIMP2, matrix metalloproteinases (MMPs), invasion worldwide [1,2]
A previous study revealed that miR-106a functions as a regulator of cell invasion, proliferation and drug sensitivity [18]. miR-106a functioned as an oncogene in human gastric cancer and contributed to proliferation and metastasis in vitro and in vivo and a high expression of miR-106a was associated with the poor survival rate of gastric cancer patients [19,20]
The expression of miR-106a was downregulated in glioma, renal carcinoma and osteosarcoma cancer [22,23,24]. miR-106a inhibited glioma cell growth by targeting E2F1 independent of p53 status [25]. miR-106a inhibited the proliferation of renal carcinoma cells by targeting IRS-2 [24]
Summary
Cervical cancer (CC) is one of the most common cancers and the third leading cause of cancer-related deaths in women. MiR‐106a, which is derived from the precursor miR-106a-363 on chromosome Xq26.2, was revealed to play a critical role in the progression of cancers [13,14,15,16,17]. A previous study revealed that miR-106a functions as a regulator of cell invasion, proliferation and drug sensitivity [18]. Upregulated expression of miR-106a by DNA hypomethylation played an oncogenic role in hepatocellular carcinoma by targeting TP53INP1 and CDKN1A [21]. The expression of miR-106a was downregulated in glioma, renal carcinoma and osteosarcoma cancer [22,23,24]. MiR-106a inhibited the proliferation of renal carcinoma cells by targeting IRS-2 [24]. MiR-106a suppressed the proliferation, migration and invasion of osteosarcoma cells by targeting HMGA2 [22]. The functional role and the underlying molecular mechanism by which miR‐106a regulates the development and progression of CC have not been elucidated
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