ROR2 promotes invasion and chemoresistance of triple-negative breast cancer cells by activating PI3K/AKT/mTOR signaling

被引:2
作者
Da, Xia [1 ]
Ge, Han [2 ]
Shi, Junfeng [3 ]
Zhu, Chunhua [1 ]
Wang, Guozhu [1 ]
Fang, Yuan [4 ]
Xu, Jin [1 ]
机构
[1] Nanjing Med Univ, Nanjing Hosp 1, Dept Breast & Thyroid Surg, Nanjing, Peoples R China
[2] Nanjing Med Univ, Affiliated Hosp 1, Dept Gen Surg, Nanjing, Peoples R China
[3] Nanjing Med Univ, Nanjing Hosp 1, Dept Oncol, Nanjing, Peoples R China
[4] Nanjing Med Univ, Nanjing Hosp 1, Dept Pathol, Nanjing, Peoples R China
关键词
Apoptosis; Metastasis; PI3K/AKT/mTOR signaling; Proliferation; Receptor tyrosine kinase-like orphan receptor 2; Triplet-negative breast cancer;
D O I
10.32604/or.2024.045433
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Objective: This study aimed to investigate the role of receptor tyrosine kinase-like orphan receptor 2 (ROR2) in triple-negative breast cancer (TNBC). Methods: ROR2 expression in primary TNBC and metastatic TNBC tissues was analyzed by immunohistochemical staining and PCR. ROR2 expression in TNBC cell lines was detected by PCR and Western blot analysis. The migration, invasion and chemosensitivity of TNBC cells with overexpression or knockdown of ROR2 were examined. Results: ROR2 expression was high in metastatic TNBC tissues. ROR2 knockdown suppressed the migration, invasion and chemoresistance of TNBC cells. ROR2 overexpression in MDAMB-435 cells promoted the migration, invasion, and chemoresistance. Moreover, ROR2 knockdown in HC1599 and MDA-MB-435 adriamycin-resistant cells enhanced chemosensitivity to adriamycin. ROR2 could activate PI3K/AKT/ mTOR signaling in TNBC cells. Conclusion: ROR2 is upregulated and promotes metastatic phenotypes of TNBC by activating PI3K/AKT/mTOR signaling.
引用
收藏
页码:1209 / 1219
页数:11
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