AEG-1 induces papillary thyroid carcinoma proliferation and metastasis by regulating cell autophagy and epithelial-mesenchymal transition
10.3760/cma.j.cn431274-20191224-01455
- VernacularTitle:AEG-1调控细胞自噬及上皮间质转化诱导甲状腺乳头状癌增殖和转移的机制研究
- Author:
Shiling HUANG
;
Weihao LIN
;
Le XIE
;
Yuansen QIN
- From:
Journal of Chinese Physician
2021;23(1):48-53,58
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To study the effect of astrocyte elevated gene-1 (AEG-1) on proliferation and metastasis of papillary thyroid cancer (PTC) by regulating cell autophagy and epithelial-mesenchymal transition (EMT).Methods:Normal thyroid cells Nthy-ori3-1 and PTC cells TPC-1, FTC-133, B-CPAP and SW579 were cultured in vitro. Real time fluorescent quantitative polymerase chain reaction (qRT-PCR) was used to detect the expression of AEG-1 in PTC cells. The PTC cells with the highest AEG-1 expression were selected for AEG-1 shRNA infection, and then divided into sh-NC group and sh-AEG-1 group. Cell counting kit-8 (CCK8) and EdU (5-ethynyl-2 ′- deoxyuridine) experiments were used to detect the effect of AEG-1 on the proliferation of PTC cells; Transwell test was used to detect the effect of AEG-1 on the metastasis of PTC cells; subcutaneous tumorigenesis test in nude mice was used to detect the effect of AEG-1 on the expression of autophagy related proteins and EMT related proteins. PTC cells in sh-NC group and sh-AEG-1 group were treated with rapamycin and transforming growth factor-β (TGF-β), respectively. CCK8 and transwell assay were used to detect the cell proliferation and metastasis ability of each group of cells, respectively. Results:Compared with normal thyroid cells Nthy-ori3-1, the expression level of AEG-1 in PTC cells was increased, with the highest expression in TPC-1 cells. After AEG-1 shRNA was transfected into TPC-1 cells, cell proliferation, metastasis and tumorigenicity in vivo were reduced ( P<0.05). Compared with the sh-NC group, the expression of autophagy-related proteins P62 and Beclin1 were increased and the expression of LC3B protein was decreased, and EMT-related proteins E-cadherin expression were increased and N-cadherin and Vimentin protein expression were decreased in the sh-AEG-1 group ( P<0.05). CCK8 and Transwell experiments showed that treatment with autophagy inducer Rapamycin and EMT inducer TGF-β attenuated the inhibitory effect of sh-AEG-1 on proliferation and metastasis ability of PTC cell ( P<0.05). Conclusions:AEG-1 promotes the proliferation and metastasis of PTC cells by inducing cell autophagy and EMT.