Autor: |
ZHANG Hong, KANG Pengpeng, CHONG Xiaoyu, HU Jingyu, ZHANG Changgeng |
Předmět: |
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Zdroj: |
Chinese Journal of Cancer Biotherapy; 2023, Vol. 30 Issue 2, p135-141, 7p |
Abstrakt: |
Objective: To investigate the expression of cellular retinoic acid binding protein 2 (CRABP2) in endometrial adenocarcinoma tissues and cells and its effects on the proliferation and invasion of endometrial adenocarcinoma cells as well as its molecular mechanism. Methods: A total of 24 pairs of endometrioid adenocarcinoma tissues and matched normal endometrial tissues were collected from Hengshui People's Hospital from June 2020 to April 2021, and human endometrial adenocarcinoma cells (An3ca and KLE) were cultured in vitro. The expression of CRABP2 in human endometrioid adenocarcinoma tissues and normal endometrial tissues was analyzed by immunohistochemistry and WB. The knockdown efficiency of CRABP2 in An3ca and KLE cells was detected by WB method, and the proliferation and invasion ability of An3ca and KLE cells after CRABP2 knockdown was detected by EDU method and Transwell assay, the expressions of key proteins related to Wnt/β-catenin pathway (β-catenin, c-Myc, cyclin-D1, MMP7 and MMP9) in An3ca and KLE cells after CRABP2 knockdown were detected by WB. The effects of CRABP2 on the growth of xenograft tumor and the expression of Ki67 and β-catenin in xenograft tumor tissues were observed in nude mice tumorigenesis assay. Results: Compared with normal endometrial tissue, the expression of CRABP2 was up-regulated in human endometrioid adenocarcinoma tissue. Expression of CRABP2 in An3ca and KLE cells decreased after transfection of shRNA targeting CRABP2 (all P<0.01). The proliferation and invasion ability of An3ca and KLE cells were decreased after CRABP2 knockdown (all P<0.01) and the Wnt/β -catenin pathway was inhibited (P<0.01). The tumor formation experiment showed that the tumor volume of transplanted tumor in nude mice decreased significantly after CRABP2 knockdown (P<0.01). Conclusion: CRABP2 can promote the proliferation and invasion of endometrioid adenocarcinoma cells by regulating theWnt/β-catenin pathway [ABSTRACT FROM AUTHOR] |
Databáze: |
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