Open Access

ARTICLE

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

XIA DA¹, HAN GE², JUNFENG SHI³, CHUNHUA ZHU¹, GUOZHU WANG¹, YUAN FANG^4,*, JIN XU^1,*
1 Department of Breast and Thyroid, Nanjing First Hospital, Nanjing Medical University, Nanjing, China
2 Department of General Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China
3 Department of Oncology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China
4 Department of Pathology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China
* Corresponding Author: YUAN FANG. Email: ; JIN XU. Email:
(This article belongs to the Special Issue: Cancer Metastasis)

Oncology Research https://doi.org/10.32604/or.2024.045433

Received 27 August 2023; Accepted 15 January 2024; Published online 28 February 2024

Abstract

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 MDA-MB-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.

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Keywords

Receptor tyrosine kinase-like orphan receptor 2; Triplet-negative breast cancer; Proliferation; Apoptosis; PI3K/AKT/mTOR signaling; Metastasis

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