XPD inhibits cell growth and invasion and enhances chemosensitivity in esophageal squamous cell carcinoma by regulating the PI3K/AKT signaling pathway.

作者: Jie Jian , Shuang Li , Li‑Zhen Liu , Li Zhen , Ling Yao

DOI: 10.3892/IJMM.2020.4593

关键词: Cyclin D1Protein kinase BPI3K/AKT/mTOR pathwayCellChemistryCancer researchCell growthSTAT3Cell cycleAkt/PKB signaling pathway

摘要: Esophageal squamous cell carcinoma (ESCC) is a lethal disease due to its high aggressiveness. The aim of the present study was investigate role xeroderma pigmentosum complementation group D (XPD) in growth and invasion ESCC elucidate potential underlying molecular mechanisms. Western blot analysis RT‑qPCR were used detect expression level XPD tissue samples adjacent normal esophageal samples. pEGFP‑N2/XPD plasmid transfected into human lines (EC9706 EC109). proliferation, apoptosis, migration EC9706 or EC109 cells assessed following transfection with overexpression plasmid. chemosensitivity cisplatin fluorouracil evaluated by CCK‑8 assay. levels phosphoinositide 3‑kinase (PI3K)/AKT, nuclear factor (NF)‑κB, Janus kinase 2 (JAK2)/signal transducer activator transcription 3 (STAT3) mitogen‑activated protein (MAPK) signaling pathway‑related genes detected western analysis. results demonstrated that markedly lower than successfully cells, inducing overexpression. A High suppressed invasion, increased apoptotic rate cells. Furthermore, significantly fluorouracil. Following overexpression, PI3K, p‑AKT, c‑Myc, Cyclin D1, Bcl‑2, vascular endothelial (VEGF) matrix metalloproteinase (MMP)‑9 downregulated, while p21 upregulated. On whole, findings demonstrate inhibits whilst also enhancing regulating PI3K/AKT pathway. may thus be an target for treatment drug resistance.

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