miRNA-1297 Induces Cell Proliferation by Targeting Phosphatase and Tensin Homolog in Testicular Germ Cell Tumor Cells

Yang, Ningning; Zhang, Jian; Tang, Qin; Guo, Jianming; Wang, Guomin

doi:10.7314/apjcp.2014.15.15.6243

Cited by 14 publications

(12 citation statements)

References 20 publications

(21 reference statements)

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“…It has been shown that these miRNAs could affect cell proliferation, progression, or metastasis in tumor cells or tumor-like skin scars (Li et al 2013;Saini et al 2014;Yang et al 2014). Our study revealed their expression in tension force-induced bone formation.…”

Section: Discussionsupporting

confidence: 49%

Integrated miRNA and mRNA expression profiling of tension force-induced bone formation in periodontal ligament cells

Chang

Lin

Luo

et al. 2015

In Vitro Cell.Dev.Biol.-Animal

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Tension force-induced bone formation is a complex biological process altered by various factors, for example miRNAs and gene regulatory network. However, we know little about critical gene regulators and their functional consequences on this complex process. The aim of this study was to determine the integrated relation between microRNA and mRNA expression in tension force-induced bone formation in periodontal ligament cells by a system biological approach. We identified 818 mRNAs and 32 miRNAs differentially expressed between cyclic tension force-stimulated human periodontal ligament cells and control cells by microarrays. By using miRNA/mRNA network analysis, protein-protein interactions network analysis, and hub analysis, we found that miR-195-5p, miR-424-5p, miR-1297, miR-3607-5p, miR-145-5p, miR-4328, and miR-224-5p were core microRNAs of tension force-induced bone formation. WDR33, HSPH1, ERBB3, RIF1, IKBKB, CREB1, FGF2, and PAG1 were identified as hubs of the PPI network, suggesting the biological significance in this process. The miRNA expression was further examined in human PDLC and animal samples by using quantitative real-time PCR. Thus, we proposed a model of tension force-induced bone formation which is co-regulated through integration of the miRNA and mRNA. This study illustrated the benefits of system biological approaches in the analysis of tension force-induced bone formation as a complex biological process. We used public information and our experimental data to do comprehensive analysis and revealed the coordination transcriptional control of miRNAs of tension force-induced bone formation.

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Section: Discussionsupporting

confidence: 49%

Integrated miRNA and mRNA expression profiling of tension force-induced bone formation in periodontal ligament cells

Chang

Lin

Luo

et al. 2015

In Vitro Cell.Dev.Biol.-Animal

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“…Moreover, miR-1297 promoted apoptosis and inhibited the proliferation and invasion of hepatocellular carcinoma cells by targeting HMGA2 (25). However, miR-1297 induced cell proliferation by targeting phosphatase and tensin homolog in testicular germ cell tumor cells (26). These data indicated that the expression level and biological effects were dependent on the type of cancer.…”

Section: Discussionmentioning

confidence: 93%

MicroRNA-1297 inhibits metastasis and epithelial-mesenchymal transition by targeting AEG-1 in cervical cancer

Wang

Guo

et al. 2017

Oncology Reports

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Abstract. Accumulating evidence has demonstrated that aberrant miRNAs contribute to cervical cancer (CC) development and progression. However, the roles of various miRNAs in CC remain to be determined. In the present study, we confirmed that a decreased miR-1297 expression was present in CC tissues and cell lines. Our clinical analysis revealed that the downregulated miR-1297 expression was significantly correlated with poor prognostic features including lymph node metastasis and lymphovascular space invasion. Moreover, we confirmed that miR-1297 was a novel independent prognostic marker for predicting the 5-year survival of CC patients. The ectopic overexpression of miR-1297 inhibited cell migration, invasion and EMT progression, while downregulated miR-1297 reversed these effects. In addition, miR-1297 regulated AEG-1 by directly binding to its 3'-UTR. In clinical samples of CC, miR-1297 was inversely correlated with AEG-1, which was upregulated in CC. Alteration of AEG-1 expression at least partially abolished the migration, invasion and EMT progression effects of miR-1297 on CC cells. In conclusion, our results indicated that miR-1297 functioned as a tumor suppressor gene in regulating the EMT and metastasis of CC via targeting of AEG-1, and may represent a novel potential therapeutic target and prognostic marker for CC.

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“…Liang et al (18) demonstrated that microRNA-1297 inhibits prostate cancer cell proliferation and invasion by targeting the AEG-1/Wnt signaling pathway. However, Li et al (20) showed that miR-1297 mediates PTEN expression and contributes to (22). Hence, the functional significance of miR-1297 in cancer initiation and progression was cancer-type specific.…”

Section: Discussionmentioning

confidence: 99%

“…However, miR-1297 mediates PTEN expression and contributes to cell progression in laryngeal squamous cell carcinoma (20). In addition, miR-1297 regulates growth of testicular germ cell tumor through PTEN/PI3K/AKT pathway (21,22). Therefore, the functional roles of miR-1297 in human cancers are cancer-type specific.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-1297 contributes to tumor growth of human breast cancer by targeting PTEN/PI3K/AKT signaling

Liu

et al. 2017

Oncology Reports

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Increasing evidence confirms that aberrant miRNA expression contributes to breast cancer (BC) development and progression. However, the roles of different miRNAs in BC remain to be explored. In the present study, we demonstrated that miR-1297 expression was increased in BC tissues and cell lines. Our clinical analysis revealed that the upregulated miR-1297 expression was significantly correlated with poor prognostic features including advanced TNM stage and larger tumor size. Moreover, we found that miR-1297 was a novel independent prognostic marker for predicting 5-year survival of BC patients. The ectopic overexpression of miR-1297 promoted cell proliferation, cell cycle progression and inhibited apoptosis while miR-1297 knockdown reversed the effect. In addition, miR-1297 modulated PTEN by directly binding to its 3'-UTR, resulting in activation of AKT signaling. In clinical samples of BC, miR-1297 inversely correlated with PTEN, which was downregulated in BC. Alternation of PTEN expression or AKT inhibitor at least partially abolished the biological effects of miR-1297 on BC cells. In conclusion, our results indicated that miR-1297 functioned as an oncogene in regulating the proliferation, cell cycle and apoptosis of BC via targeting PTEN/PI3K/AKT signaling, and may represent a novel potential therapeutic target and prognostic marker for BC.

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miRNA-1297 Induces Cell Proliferation by Targeting Phosphatase and Tensin Homolog in Testicular Germ Cell Tumor Cells

Cited by 14 publications

References 20 publications

Integrated miRNA and mRNA expression profiling of tension force-induced bone formation in periodontal ligament cells

Integrated miRNA and mRNA expression profiling of tension force-induced bone formation in periodontal ligament cells

MicroRNA-1297 inhibits metastasis and epithelial-mesenchymal transition by targeting AEG-1 in cervical cancer

MicroRNA-1297 contributes to tumor growth of human breast cancer by targeting PTEN/PI3K/AKT signaling

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