We are analyzing https://link.springer.com/article/10.1007/s11626-016-0093-2.

Title:
Upregulated microRNA-224 promotes ovarian cancer cell proliferation by targeting KLLN | In Vitro Cellular & Developmental Biology - Animal
Description:
Human epithelial ovarian cancer is a complex disease, with low 5-yr survival rate largely due to the terminal stage at diagnosis in most patients. MicroRNAs play critical roles during epithelial ovarian cancer progression in vivo and have also been shown to regulate characteristic of ovarian cancer cell line in vitro. Alterative microRNA-224 (microRNA-224) expression affects human epithelial ovarian cancer cell survival, apoptosis, and metastasis. However, people know little about the effects of microRNA-224 on epithelial ovarian cancer cell proliferation. In the current study, we found that the microRNA-224 expression level of human syngeneic epithelial ovarian cancer cells HO8910 (low metastatic ability) was lower than that of HO8910PM (high metastatic ability). Furthermore, microRNA-224 was confirmed to target KLLN in HO8910 and HO8910PM. The known KLLN downstream target cyclin A was regulated by microRNA-224 in HO8910 and HO8910PM. In addition, overexpression of microRNA-224 enhanced the proliferation abilities of HO8910 and knockdown of microRNA-224 suppressed the proliferation abilities of HO8910PM by KLLN-cyclin A pathway. Our results provide new data about microRNAs and their targets involved in proliferation of epithelial ovarian cancer cells by modulating the downstream signaling.
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Keywords {🔍}

cancer, ovarian, microrna, article, cell, pubmed, human, google, scholar, epithelial, cas, cells, proliferation, klln, liang, expression, wang, micrornas, esm, docx, progression, apoptosis, hopm, access, yang, mol, oncol, privacy, cookies, content, targeting, meng, chen, zhang, breast, data, information, publish, research, search, vitro, cellular, targets, small, liu, int, natl, inhibits, eng, hum,

Topics {✒️}

month download article/chapter klln epigenotype-phenotype associations ovarian cancer cells epithelial ovarian cancer ovarian cancer progression granulosa cell function p53-regulated nuclear inhibitor ovarian epithelial tumours ovarian cancer biomarkers meng liang carried full article pdf microrna-224 inhibits progression electronic supplementary material human cervical cancer low metastatic ability control cell invasion cellular signaling modulated human prostate cancer microrna epigenetic alterations privacy choices/manage cookies profiling microrna expression article hu ke hu microrna-224 expression level mir-141 regulates keap1 cell cycle control epithelial-mesenchymal transition high metastatic ability van kuijk pf van ijcken wf vitro cell future promise ovarian cancer somatic klln alterations meng liang small rnas candidate microrna biomarkers modulates cisplatin sensitivity microrna-224-specific target original cisplatin resistance sumoylation-independent manner european economic area unveiling mechanistic pathways plasminogen activator inhibitor-1 drug transporter abcb9 conserved seed pairing pancreatic ductal adenocarcinomas tp53/tp73 stimulation human cancer microrna-224 targets rkip

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         description:Human epithelial ovarian cancer is a complex disease, with low 5-yr survival rate largely due to the terminal stage at diagnosis in most patients. MicroRNAs play critical roles during epithelial ovarian cancer progression in vivo and have also been shown to regulate characteristic of ovarian cancer cell line in vitro. Alterative microRNA-224 (microRNA-224) expression affects human epithelial ovarian cancer cell survival, apoptosis, and metastasis. However, people know little about the effects of microRNA-224 on epithelial ovarian cancer cell proliferation. In the current study, we found that the microRNA-224 expression level of human syngeneic epithelial ovarian cancer cells HO8910 (low metastatic ability) was lower than that of HO8910PM (high metastatic ability). Furthermore, microRNA-224 was confirmed to target KLLN in HO8910 and HO8910PM. The known KLLN downstream target cyclin A was regulated by microRNA-224 in HO8910 and HO8910PM. In addition, overexpression of microRNA-224 enhanced the proliferation abilities of HO8910 and knockdown of microRNA-224 suppressed the proliferation abilities of HO8910PM by KLLN-cyclin A pathway. Our results provide new data about microRNAs and their targets involved in proliferation of epithelial ovarian cancer cells by modulating the downstream signaling.
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      description:Human epithelial ovarian cancer is a complex disease, with low 5-yr survival rate largely due to the terminal stage at diagnosis in most patients. MicroRNAs play critical roles during epithelial ovarian cancer progression in vivo and have also been shown to regulate characteristic of ovarian cancer cell line in vitro. Alterative microRNA-224 (microRNA-224) expression affects human epithelial ovarian cancer cell survival, apoptosis, and metastasis. However, people know little about the effects of microRNA-224 on epithelial ovarian cancer cell proliferation. In the current study, we found that the microRNA-224 expression level of human syngeneic epithelial ovarian cancer cells HO8910 (low metastatic ability) was lower than that of HO8910PM (high metastatic ability). Furthermore, microRNA-224 was confirmed to target KLLN in HO8910 and HO8910PM. The known KLLN downstream target cyclin A was regulated by microRNA-224 in HO8910 and HO8910PM. In addition, overexpression of microRNA-224 enhanced the proliferation abilities of HO8910 and knockdown of microRNA-224 suppressed the proliferation abilities of HO8910PM by KLLN-cyclin A pathway. Our results provide new data about microRNAs and their targets involved in proliferation of epithelial ovarian cancer cells by modulating the downstream signaling.
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