AI Article Synopsis
- * Methods involved analyzing ROR2 expression using various techniques and assessing the effects of ROR2 overexpression and knockdown on cell behavior and drug response.
- * Results showed that ROR2 promotes migration, invasion, and drug resistance in TNBC cells, activating the PI3K/AKT/mTOR signaling pathway.
Article 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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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11209745 | PMC |
| http://dx.doi.org/10.32604/or.2024.045433 | DOI Listing |
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