MicroRNA-200c plays an oncogenic role in nasopharyngeal carcinoma by targeting PTEN

Zhang, Zhenzhen; Cao, Heng-Chang; Huang, Dongli; Wu, Qi; Chen, Xiaofan; Wan, Jun; Zhang, Wei

doi:10.1177/1010428317703655

Cited by 9 publications

(7 citation statements)

References 37 publications

(39 reference statements)

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“…It has been reported that PTEN was a direct target of miR-200b and miR-200c in endometrial cancer and nasopharyngeal carcinoma [28, 29]. In addition, a growing number of studies indicated that PTEN played an important role in the abnormal proliferation of PCOS GCs [30, 31].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-200b and microRNA-200c are up-regulated in PCOS granulosa cell and inhibit KGN cell proliferation via targeting PTEN

Sun

Zhang

et al. 2019

Reprod Biol Endocrinol

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Background Polycystic ovary syndrome (PCOS) is one of the most common endocrine metabolic disorders characterized by hyperandrogenism, polycystic ovaries and ovulatory dysfunction. Several studies have reported that the aberrant expression of miRNAs contributes a lot to disordered folliculogenesis in PCOS, though the role and underlying mechanism of microRNA-200b (miR-200b) and microRNA-200c (miR-200c) in the development of PCOS remain unclear. Methods The expression of miR-200b in granulosa cells (GCs) derived from 90 PCOS patients and 70 controls was analyzed by using quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Granulosa-like tumor cell line (KGN) was cultured for cell counting kit-8 (CCK-8) assays after over-expression of miR-200b, miR-200c or knockdown phosphatase and tensin homolog (PTEN). TargetScan was used to identify the potential targets of miR-200b and miR-200c, which was further verified by qRT-PCR, western blot and luciferase assays. Results Significantly increased expression of miR-200b was observed in PCOS patients compared with the controls. Moreover, over-expression of miR-200b and miR-200c inhibited the proliferation of KGN cells. In addition, our results verified that miR-200b and miR-200c directly targeted PTEN, knockdown of which suppressed KGN cells proliferation. Conclusion Our findings demonstrate that miR-200b and miR-200c suppress the proliferation of KGN cells by targeting PTEN, and this might provide new evidence for abnormal proliferation of GCs in PCOS.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-200b and microRNA-200c are up-regulated in PCOS granulosa cell and inhibit KGN cell proliferation via targeting PTEN

Sun

Zhang

et al. 2019

Reprod Biol Endocrinol

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“…PTEN is a well-characterized tumor suppressor gene, which antagonizes the phosphoinositol-3-kinase/protein kinase B (PKB or Akt) signaling pathway [ 12 ]. The PTEN gene acts as a tumor suppressor gene in multiple cancers, including breast cancer [ 13 , 14 ], nasopharyngeal carcinoma [ 15 ], renal cell carcinoma [ 16 ], non-small-cell lung cancer [ 17 ], hepatocellular carcinoma [ 18 ], human NK/T-cell lymphoma [ 19 ], and osteosarcoma [ 20 ]. The loss of function of PTEN in tumor cells results in the accumulation of critical cell messengers, which increases Akt phosphorylation and activity and leads to decreased apoptosis and/or increased mitogenic signaling [ 21 , 22 ].…”

Section: Introductionmentioning

confidence: 99%

Shikonin Inhibites Migration and Invasion of Thyroid Cancer Cells by Downregulating DNMT1

et al. 2018

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BackgroundShikonin is a component of Chinese herbal medicine. The aim of this study was to investigate the effects of shikonin on cell migration of papillary thyroid cancer cells of the TPC-1 cell line in vitro and expression levels of the phosphate and tensin homolog deleted on chromosome 10 (PTEN) and DNA methyltransferase 1 (DNMT1) genes.Material/MethodsThe Cell Counting Kit-8 (CCK-8) assay was performed to evaluate the proliferation of TPC-1 papillary thyroid cancer cells, and the normal thyroid cells, HTori-3, in vitro. A transwell motility assay was used to analyze the migration of TPC-1 cells. Western blot was performed to determine the expression levels of PTEN and DNMT1 genes. A methylation-specific polymerase chain reaction (PCR) (MSP) assay was used to evaluate the methylation of PTEN.ResultsFollowing treatment with shikonin, the cell survival rate of TPC-1 cells decreased in a dose-dependent manner; the inhibitory effects on HTori-3 cells were less marked. Shikonin inhibited TPC-1 cell migration and invasion in a dose-dependent manner. The methylation of PTEN was suppressed by shikonin, which also reduced the expression of DNMT1 in a dose-dependent manner, and increased the expression of PTEN. Overexpression of DNMT1 promoted the migration of TPC-1 cells and the methylation of PTEN. Levels of protein expression of PTEN in TPC-1 cells treated with shikonin decreased, and were increased by DNMT1 knockdown.ConclusionsShikonin suppressed the expression of DNMT1, reduced PTEN gene methylation, and increased PTEN protein expression, leading to the inhibition of TPC-1 cell migration.

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“… 12 Notably, miRNAs were reported to regulate EMT in a number of studies. For example, the miR-200 family was shown to directly target Nanog to inhibit EMT, but may play an oncogenic role in NPC, 13 , 14 whereas miR-30 was shown to target Snail1 to inhibit invasion and metastasis in the regulation of EMT. 15 …”

Section: Introductionmentioning

confidence: 99%

MicroRNA-328 inhibits migration and epithelial–mesenchymal transition by targeting CD44 in nasopharyngeal carcinoma cells

Lin

Chiang

Chen

2018

OTT

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BackgroundMicroRNAs (miRNAs) play crucial roles in various types of cancers, particularly in tumor development, migration, and progression. Dysregulation of miR-328 was reported to occur in some types of human malignancies, however, the role of miR-328 in nasopharyngeal carcinoma (NPC) and its potential involvement in metastasis remain undetermined.MethodsThe invasion capacity of NPC sphere-forming cells was evaluated by in vitro cell migration assays. Differential miRNAs expression was examined in NPC sphere-forming cells compared to parental monolayer cells using miRNA array analysis. The role of miR-328 in regulating NPC cells migratory properties was analyzed after miR-328 mimics transfection. The expression of E-cadherin and CD44 was analyzed by flow cytometry. CD44 was examined as a target of miR-328 through luciferase reporter assays and Western blotting.ResultsHere, we report that NPC TW01 and TW06 sphere-forming cells exhibited increased migratory ability in comparison with parental monolayer cells. Sphere-forming cells had significantly lower levels of miR-328, as observed using miRNA arrays and confirmed through real-time polymerase chain reaction. Overexpression of miR-328 induced by transfection with synthetic miR-328 mimics decreased the migration of NPC sphere-forming cells. The inhibitory effects were associated with increased expression of E-cadherin and the downregulated expression of mesenchymal markers such as N-cadherin, Snail, and vimentin. Moreover, our results demonstrated that miR-328 suppressed NPC cell migration and inhibited the epithelial–mesenchymal transition process directly through a binding site on the CD44 3′ untranslated region.ConclusionmiR-328, a previously unrecognized miRNA, may serve as a potential prognostic marker and therapeutic target for NPC.

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MicroRNA-200c plays an oncogenic role in nasopharyngeal carcinoma by targeting PTEN

Abstract: Recent studies suggested that microRNA-200 family microRNAs play critical roles in cancer initiation and metastasis. The underlying mechanism remained elusive. In this study, we show that microRNA-200c is upregulated in nasopharyngeal carcinoma cells.

Cited by 9 publications

References 37 publications

MicroRNA-200b and microRNA-200c are up-regulated in PCOS granulosa cell and inhibit KGN cell proliferation via targeting PTEN

MicroRNA-200b and microRNA-200c are up-regulated in PCOS granulosa cell and inhibit KGN cell proliferation via targeting PTEN

Shikonin Inhibites Migration and Invasion of Thyroid Cancer Cells by Downregulating DNMT1

MicroRNA-328 inhibits migration and epithelial–mesenchymal transition by targeting CD44 in nasopharyngeal carcinoma cells

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MicroRNA-200c plays an oncogenic role in nasopharyngeal carcinoma by targeting PTEN

Abstract: Recent studies suggested that microRNA-200 family microRNAs play critical roles in cancer initiation and metastasis. The underlying mechanism remained elusive. In this study, we show that microRNA-200c is upregulated in nasopharyngeal carcinoma cells.

Cited by 9 publications

References 37 publications

MicroRNA-200b and microRNA-200c are up-regulated in PCOS granulosa cell and inhibit KGN cell proliferation via targeting PTEN

MicroRNA-200b and microRNA-200c are up-regulated in PCOS granulosa cell and inhibit KGN cell proliferation via targeting PTEN

Shikonin Inhibites Migration and Invasion of Thyroid Cancer Cells by Downregulating DNMT1

MicroRNA-328 inhibits migration and epithelial&ndash;mesenchymal transition by targeting CD44 in nasopharyngeal carcinoma cells

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MicroRNA-328 inhibits migration and epithelial–mesenchymal transition by targeting CD44 in nasopharyngeal carcinoma cells