MicroRNA-106a regulates phosphatase and tensin homologue expression and promotes the proliferation and invasion of ovarian cancer cells

Chen, Liang; Zhang, Fang; Sheng, Xiugui; Zhang, Shiqian; Chen, Yueting; Liu, Bowen

doi:10.3892/or.2016.5010

Cited by 23 publications

(19 citation statements)

References 44 publications

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“…and amplified region, and are implicated in tumorigenesis and tumor development (11). miRNAs are also involved in modulating different cancer-related biological processes, such as cell proliferation, cycle, apoptosis, angiogenesis, invasion, migration and metastasis (12)(13)(14). Moreover, numerous miRNAs are aberrantly expressed in various kinds of human cancers, such as EOC (15), cervical cancer (16), gastric cancer (17), lung cancer (18) and bladder cancer (19).…”

Section: Microrna-455 Inhibits Cell Proliferation and Invasion Of Epimentioning

confidence: 99%

MicroRNA-455 inhibits cell proliferation and invasion of epithelial ovarian cancer by directly targeting Notch1

et al. 2017

Molecular Medicine Reports

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Ovarian cancer (OC) is the fifth leading cause of cancer‑associated mortality among women in developed countries. Numerous microRNAs are aberrantly expressed in epithelial (E) OC, and are involved in EOC formation and progression. As such, microRNAs may be investigated as diagnostic and prognostic molecular biomarkers, and therapeutic targets for patients with EOC. For instance, microRNA‑455 (miR‑455) is abnormally expressed in various types of human cancer. However, details on the expression level, biological roles and underlying mechanism of miR‑455 in EOC remain unclear. In the present study, the expression of miR‑455 in EOC was detected, and its association with clinical characteristics was analysed. The functional roles and underlying mechanisms of miR‑455 in EOC were also investigated. The results revealed that miR‑455 expression in EOC tissues and cell lines was significantly downregulated. Furthermore, miR‑455 downregulation was correlated with tumor size, International Federation of Gynecology and Obstetrics stage and lymph node metastasis of patients with EOC. Restoration of miR‑455 expression efficiently inhibited cell proliferation and invasion in vitro. Notch1 was identified as a direct target of miR‑455 in EOC. The mRNA and protein expression levels of Notch1 were higher in EOC tissues compared with in normal ovarian epithelial tissues. Spearman's correlation analysis indicated that miR‑455 expression was negatively correlated with the mRNA level of Notch1 in EOC tissues. Notch1 overexpression was able to restore the EOC cell proliferation and invasion abilities suppressed by miR‑455. The present study provided evidence that the dysregulation of the miR‑455/Notch1 signalling pathway may be essential for EOC occurrence and development. In addition, the results confirmed the tumor‑suppressive roles of miR‑455 in modulating EOC proliferation and invasion through regulation of Notch1 expression. Thus, miR‑455 may be a novel miRNA‑based therapeutic target to treat patients with EOC.

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Section: Microrna-455 Inhibits Cell Proliferation and Invasion Of Epimentioning

confidence: 99%

MicroRNA-455 inhibits cell proliferation and invasion of epithelial ovarian cancer by directly targeting Notch1

et al. 2017

Molecular Medicine Reports

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“…Emerging data have demonstrated that the abnormal expression of miRNAs contributes to a number of diverse biological and pathological processes in cancer cells, including in cell proliferation, cell cycle, differentiation, development, apoptosis, migration, invasion and metastasis (12)(13)(14). Previous studies have revealed that miRNAs are involved in the carcinogenesis and progression of several types of human cancer as either oncogenes or tumor suppressors, depending on the functions of their target mRNAs (15)(16)(17). The inactivation of oncogenic miRNAs, or restoration of tumor suppressing miRNAs, has demonstrated potential in providing therapeutic treatments for patients with cancer, and the strategies are undergoing clinical trials (18)(19)(20)(21)(22).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑216b regulated proliferation and invasion of non‑small cell lung cancer by targeting SOX9

et al. 2018

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Abstract. Micro (mi)RNAs are small, evolutionarily conserved and endogenous noncoding RNA molecules between 19 and 24 nucleotides in length. The potential roles of miRNAs in the carcinogenesis and progression of non-small cell lung cancer (NSCLC) have been studied previously. In the present study, it was revealed that miRNA-216b (miR-216b) expression was lower in NSCLC tissue and cell lines compared with that in adjacent healthy lung tissue samples and the normal bronchial epithelial 16HBE cell line, respectively. The ectopic expression of miR-216b inhibited the proliferation and invasion of NSCLC cells in vitro. SRY-Box 9 (SOX9) was identified as a direct target of miR-216b in NSCLC. In addition, SOX9 small interfering RNA was able to mimic the effects of miR-216b overexpression on cell proliferation and invasion in NSCLC. Therefore, the data reported in the present study demonstrate that miR-216b is an important tumor suppressor in NSCLC. These data may contribute to the understanding of the molecular mechanism underlying the carcinogenesis and progression of NSCLC, and provide novel therapies for patients with NSCLC.

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“…Recently, 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). 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).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-106a promotes cell migration and invasion by targeting tissue inhibitor of matrix metalloproteinase 2 in cervical cancer

Zhou

Tao

et al. 2017

Oncology Reports

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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.

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MicroRNA-106a regulates phosphatase and tensin homologue expression and promotes the proliferation and invasion of ovarian cancer cells

Cited by 23 publications

References 44 publications

MicroRNA-455 inhibits cell proliferation and invasion of epithelial ovarian cancer by directly targeting Notch1

MicroRNA-455 inhibits cell proliferation and invasion of epithelial ovarian cancer by directly targeting Notch1

MicroRNA‑216b regulated proliferation and invasion of non‑small cell lung cancer by targeting SOX9

MicroRNA-106a promotes cell migration and invasion by targeting tissue inhibitor of matrix metalloproteinase 2 in cervical cancer

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