RETRACTED: AIB1 induces epithelial-mesenchymal transition in gastric cancer via the PI3K/AKT signaling (Retracted article. See vol. 122, pg. 1973, 2021)

被引:7
作者
Diao, Lei [1 ]
Li, Yang [1 ]
Mei, Qiao [1 ]
Han, Wei [1 ]
Hu, Jing [1 ]
机构
[1] Anhui Med Univ, Affiliated Hosp 1, Dept Gastroenterol, 218 Jixi Rd, Hefei 230022, Anhui, Peoples R China
关键词
AIB1; epithelial-mesenchymal transition; gastric cancer; PI3K; AKT signaling; RECEPTOR COACTIVATOR AIB1; CELL-PROLIFERATION; PROGRESSION; ACTIVATION; PATHWAYS; SRC-3; AKT; OVEREXPRESSION; AMPLIFICATION; EXPRESSION;
D O I
10.1002/jcb.29530
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Amplified in breast cancer 1 (AIB1) is overexpression in various cancers and promotes tumor cell proliferation, survival, and invasiveness. However, the role of AIB1 in the regulation of gastric cancer (GC) cell epithelial-mesenchymal transition (EMT) is still largely unclear. In the present study, immunohistochemistry showed that AIB1 was upregulated in our cohort of patients with GC and correlated with poor survival. Knockdown of AIB1 reduced the invasive ability of GC cells, downregulated the expression of epithelial cell marker E-cadherin, and upregulated mesenchymal cell marker vimentin. AIB1 overexpression elicited the opposite effect. PI-103, the inhibitor of the PI3K/AKT signaling, partially reversed AIB1 overexpression mediated a decrease in E-cadherin and an increase in vimentin. The present data demonstrated that AIB1 augmented the EMT via activation of PI3K/AKT signaling. In conclusion, our results suggested a novel role of AIB1 in GC invasion and EMT and raised the possibility of using this molecule as an indicator for GC treatment.
引用
收藏
页码:926 / 933
页数:8
相关论文
共 23 条
[1]   Genes and proteins involved in mesenchymal to epithelial transition [J].
Barasch, J .
CURRENT OPINION IN NEPHROLOGY AND HYPERTENSION, 2001, 10 (03) :429-436
[2]   Snail1 induces epithelial-to-mesenchymal transition and tumor initiating stem cell characteristics [J].
Dang, Hien ;
Ding, Wei ;
Emerson, Dow ;
Rountree, C. Bart .
BMC CANCER, 2011, 11
[3]   Gastric adenocarcinoma - Review and considerations for future directions [J].
Dicken, BJ ;
Bigam, DL ;
Cass, C ;
Mackey, JR ;
Joy, AA ;
Hamilton, SM .
ANNALS OF SURGERY, 2005, 241 (01) :27-39
[4]   Cancer metastases: challenges and opportunities [J].
Guan, Xiangming .
ACTA PHARMACEUTICA SINICA B, 2015, 5 (05) :402-418
[5]   Overexpression of the nuclear receptor coactivator AIB1, (SRC-3) during progression of pancreatic adenocarcinoma [J].
Henke, RT ;
Haddad, BR ;
Kim, SE ;
Rone, JD ;
Mani, A ;
Jessup, JM ;
Wellstein, A ;
Maitra, A ;
Riegel, AT .
CLINICAL CANCER RESEARCH, 2004, 10 (18) :6134-6142
[6]   Cisplatin Treatment of Primary and Metastatic Epithelial Ovarian Carcinomas Generates Residual Cells With Mesenchymal Stem Cell-Like Profile [J].
Latifi, Ardian ;
Abubaker, Khalid ;
Castrechini, Natalie ;
Ward, Alister C. ;
Liongue, Clifford ;
Dobill, Francoise ;
Kumar, Janani ;
Thompson, Erik W. ;
Quinn, Michael A. ;
Findlay, Jock K. ;
Ahmed, Nuzhat .
JOURNAL OF CELLULAR BIOCHEMISTRY, 2011, 112 (10) :2850-2864
[7]   Activation of β-catenin and Akt pathways by Twist are critical for the maintenance of EMT associated cancer stem cell-like characters [J].
Li, Junlin ;
Zhou, Binhua P. .
BMC CANCER, 2011, 11
[8]   Amplified in breast cancer 1 promotes colorectal cancer progression through enhancing notch signaling [J].
Mo, P. ;
Zhou, Q. ;
Guan, L. ;
Wang, Y. ;
Wang, W. ;
Miao, M. ;
Tong, Z. ;
Li, M. ;
Majaz, S. ;
Liu, Y. ;
Su, G. ;
Xu, J. ;
Yu, C. .
ONCOGENE, 2015, 34 (30) :3935-3945
[9]   AIB1:ERα Transcriptional Activity Is Selectively Enhanced in Aromatase Inhibitor-Resistant Breast Cancer Cells [J].
O'Hara, Jane ;
Vareslija, Damir ;
McBryan, Jean ;
Bane, Fiona ;
Tibbitts, Paul ;
Byrne, Christopher ;
Conroy, Ronan M. ;
Hao, Yuan ;
Gaora, Peadar O. ;
Hill, Arnold D. K. ;
McIlroy, Marie ;
Young, Leonie S. .
CLINICAL CANCER RESEARCH, 2012, 18 (12) :3305-3315
[10]   The nuclear receptor coactivator AIB1 mediates insulin-like growth factor I-induced phenotypic changes in human breast cancer cells [J].
Oh, A ;
List, HJ ;
Reiter, R ;
Mani, A ;
Zhang, Y ;
Gehan, E ;
Wellstein, A ;
Riegel, AT .
CANCER RESEARCH, 2004, 64 (22) :8299-8308