MORC2/β-catenin signaling axis promotes proliferation and migration of breast cancer cells

Although Microrchidia 2 (MORC2) is overexpressed in many types of human cancer, its role in breast cancer progression remains unknown. Here, we report that the chromatin remodeler MORC2 expression positively correlates with β-catenin expression in breast cancer cell lines and patients. Overexpressio...

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Bibliographic Details
Published in:Medical oncology (Northwood, London, England) London, England), 2022-09, Vol.39 (9), p.135-135, Article 135
Main Authors: Saroha, Himanshu Singh, Kumar Guddeti, Rohith, Jacob, Jasmine P., Kumar Pulukuri, Kiran, Karyala, Prashanthi, Pakala, Suresh B.
Format: Article
Language:English
Subjects:
Antibodies
Breast cancer
Cell growth
Gene expression
Hematology
Internal Medicine
Kinases
Medical prognosis
Medicine
Medicine & Public Health
Metastasis
Mutation
Oncology
Original Paper
Pathology
Phosphorylation
Proteins
Science education
Wound healing
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Summary:Although Microrchidia 2 (MORC2) is overexpressed in many types of human cancer, its role in breast cancer progression remains unknown. Here, we report that the chromatin remodeler MORC2 expression positively correlates with β-catenin expression in breast cancer cell lines and patients. Overexpression of MORC2 augmented the expression of β-catenin and its target genes, cyclin D1 and c-Myc. Consistent with these results, we found MORC2 knockdown resulted in decreased expression of β-catenin and its target genes. Surprisingly, we observed that c-Myc, the target gene of β-catenin, regulated the MORC2-β-catenin signaling axis through a feedback mechanism. We demonstrated that MORC2 regulates β-catenin expression and function by modulating the phosphorylation of AKT. In addition, we observed reduced proliferation and migration of MORC2 overexpressing breast cancer cells upon β-catenin inhibition. Overall, our results demonstrate that MORC2 promotes breast cancer cell proliferation and migration by regulating β-catenin signaling.
ISSN:1559-131X
1357-0560
1559-131X
DOI:10.1007/s12032-022-01728-6