miR-195 inhibits esophageal cancer cell proliferation via targeting cyclin D1 and Cdc42 - 13/11/19
, Qianshun Chen b , Xunyu Xu b, ⁎ , Xu Wu a, ⁎ Bienvenue sur EM-consulte, la référence des professionnels de santé.
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Abstract |
Background |
MiR-195 plays an important role in metastasis and invasion of esophageal cancer (EC). However, the specific mechanism is not clear. The aim of this study was to explore the pathways how miR-195 controls EC cell proliferation.
Method |
Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was applied to detect theexpression of miR-195 in 25 cases of EC tissues and matched adjacent normal tissues in EC patients. MTT, colony formation and flow cytometry were performed to evaluate the effects of miR-195 on cell proliferation, respectively. Dual luciferase reporter assay was used to verify that cyclin D1 and cdc42 were targets of miR-195. qRT-PCR and western blot analysis were performed to analyze mRNA and protein expression.
Result |
In this study, we observed that miR-195 was repressed in EC tissue than in normal tissue. Similarly, miR-195 also showed lower expressions in EC cell lines (ECA109, TE-1, TE-8 and TE-13) than in the primary human esophageal epithelial cell (HEEC). Overexpression of miR-195 inhibited EC cell proliferation while treatment of antagomir promoted EC cell proliferationby suppressed Cdc42 and cyclin D1.
Conclusion |
Our result indicated miR-195 suppresses cyclin D1 and Cdc42 to inhibit EC cell proliferation, and Cdc42 may via regulating both cyclin D1-dependent and independent pathways to control EC cell proliferation.
Le texte complet de cet article est disponible en PDF.Abbreviations : EC, HEEC, ESCC, EAC, CDKs, Rb, STAT3, ERKs, Cdc42, MAPK, JNK, CREB, miRNA
Keywords : miR-195, Esophageal cancer, Cell proliferation, Cyclin D1, Cdc42
Plan
Vol 120
Article 109525- décembre 2019 Retour au numéro
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