Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0598934 (tumor growth)
 58,965 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Endometrial cancer (EC), a prevalent gynecologic tumor, is a great threat to women. We aimed to explore miR-142's effects on EC and the relevant mechanisms. Cell proliferation was evaluated with MTT, cell counting, and colony formation assay. MRNA abundances of miR-142 and cyclin D1 (CCND1) were examined with quantitative real-time PCR. CCND1 protein level in cells was analyzed with Western blot. miR-142's downstream target was identified with targetscan and luciferase reporter assay. Nude mice were injected subcutaneously with Ishikawa (ISK) cells transfected with or without miR-142 mimics. Ki-67 and CCND1 expressions in tumors of xenograft mice were analyzed with immunohistochemical assay. miR-142 was expressed at a lower level in human EC tumor samples than matched normal tissues, and its mRNA level in EC patients without metastasis was higher than that in patients with metastatic EC. Additionally, low-level miR-142 was closely linked with the poor prognosis of EC patients. miR-142 restricted ISK and HEC-1A cell proliferation. Targetscan and luciferase reporter assay proved the target relationship between miR-142 and CCND1. Moreover, high-level CCND1 was positively correlated with the poor prognosis of EC patients. Besides, miR-142 mimics restricted tumor growth in ISK xenografted mice, as well as inhibited the expression of Ki67 and CCND1 in excised tumors. miR-142 restricted EC proliferation by targeting CCND1.
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PMID:miR-142 Suppresses Endometrial Cancer Proliferation In Vitro and In Vivo by Targeting Cyclin D1. 3058 37

Puerarin has recently been demonstrated to play anti-cancer roles in a series of human cancers, including non-small cell lung cancer (NSCLC), possibly through regulation of cancer-related microRNAs (miRNAs). The purpose of the present study was to further investigate the detailed role and underlying mechanism of puerarin on NSCLC progression. Cell viability and apoptosis were assessed using the Cell Counting kit-8 (CCK-8) assay and flow cytometry, respectively. Transwell assays were performed to determine cell migration and invasion abilities. The qRT-PCR assay was employed to detect the expression of miR-342 and cyclin D1 (CCND1) mRNA, and CCND1 protein expression was evaluated by western blotting. The targeted interaction between miR-342 and CCND1 was verified by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. We found that our data demonstrated that puerarin repressed cell viability, migration, invasion, and cell cycle progression, and enhanced the apoptosis of NSCLC cells. miR-342 overexpression hindered the migration, invasion and cell cycle progression, and accelerated the apoptosis of NSCLC cells. miR-342 inhibited CCND1 expression by directly binding to the 3'-UTR of CCND1. Moreover, miR-342 overexpression-mediated anti-migration, anti-invasion, anti-cell cycle progression, and pro-apoptotic effects were abated by co-transfection of pcDNA-CCND1. More importantly, puerarin inhibited CCND1 expression by upregulating miR-342. Additionally, puerarin hampered NSCLC cell progression in vitro and tumor growth in vivo by upregulating miR-342. In conclusion, our study suggested that puerarin hampered NSCLC progression in vitro and in vivo at least partly through regulating miR-342/CCND1 axis, highlighting a novel mechanism of puerarin exerting anti-cancer property in NSCLC.
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PMID:Puerarin alleviates the progression of non-small cell lung cancer by regulating the miR-342/CCND1 axis. 3274 50