Journal
CELL DEATH & DISEASE
Volume 12, Issue 10, Pages -Publisher
SPRINGERNATURE
DOI: 10.1038/s41419-021-04133-5
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Funding
- NIH/NCI [R01 CA211696-01A1, R01CA211696-02S1]
- NIH/NCATS Colorado CTSA Grant [TL1 TR002533]
- ACS [RSG-16-171-010CSM]
- Department of Medicine Outstanding Early Career Scholars Award
- University of Colorado Cancer Center Support Grant [P30CA046934]
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The study reveals that SEMA7A promotes anoikis resistance in mammary epithelial cells and plays a role during mammary gland involution. SEMA7A is primarily expressed in cells expressing alpha 6-integrin, and a decrease in luminal progenitor cells is observed in SEMA7A-/- mice during involution.
Semaphorin-7a (SEMA7A), best known as a neuroimmune molecule, plays a diverse role in many cellular processes and pathologies. Here, we show that SEMA7A promotes anoikis resistance in cultured mammary epithelial cells through integrins and activation of pro-survival kinase AKT, which led us to investigate a role for SEMA7A during postpartum mammary gland involution-a normal developmental process where cells die by anoikis. Our results reveal that SEMA7A is expressed on live mammary epithelial cells during involution, that SEMA7A expression is primarily observed in alpha 6-integrin expressing cells, and that luminal progenitor cells, specifically, are decreased in mammary glands of SEMA7A-/- mice during involution. We further identify a SEMA7A-alpha 6/beta 1-integrin dependent mechanism of mammosphere formation and chemoresistance in mammary epithelial cells and suggest that this mechanism is relevant for recurrence in breast cancer patients.
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