scholarly journals Anoikis resistance in mammary epithelial cells is mediated by semaphorin 7a

2021 ◽  
Vol 12 (10) ◽  
Author(s):  
Taylor R. Rutherford ◽  
Alan M. Elder ◽  
Traci R. Lyons
Keyword(s):  
Epithelial Cells ◽  
Developmental Process ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Breast Cancer Patients ◽  
Anoikis Resistance ◽  
Mammosphere Formation ◽  
Cellular Processes ◽  
Luminal Progenitor Cells ◽  
Dependent Mechanism

AbstractSemaphorin-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 α6-integrin expressing cells, and that luminal progenitor cells, specifically, are decreased in mammary glands of SEMA7A−/− mice during involution. We further identify a SEMA7A-α6/β1-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.

scholarly journals Anoikis resistance in mammary epithelial cells is mediated by semaphorin-7a.

2021 ◽  
Author(s):  
Taylor Renee Rutherford ◽  
Alan M Elder ◽  
Traci R Lyons
Keyword(s):  
Epithelial Cells ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Breast Cancer Patients ◽  
Anoikis Resistance ◽  
Mammosphere Formation ◽  
Cellular Processes ◽  
Mammary Gland Involution ◽  
Luminal Progenitor Cells ◽  
Dependent Mechanism

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 integrin mediated activation of pro-survival kinase AKT, which led us to investigate a role for SEMA7A during postpartum mammary gland involution- a normal process in development 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 a6-integrin expressing cells, and that luminal progenitor cells, specifically, are decreased in mammary glands of SEMA7A-/- mice during involution. We further identify a SEMA7A/b1-integrin dependent mechanism of cell survival that promotes anoikis resistance, mammosphere formation, and chemoresistance in mammary epithelial cells and suggest that this mechanism is relevant for recurrence in breast cancer patients.

scholarly journals ErbB2 requires integrin  5 for anoikis resistance via Src regulation of receptor activity in human mammary epithelial cells

2010 ◽  
Vol 123 (8) ◽  
pp. 1373-1382 ◽  
Author(s):  
K. K. Haenssen ◽  
S. A. Caldwell ◽  
K. S. Shahriari ◽  
S. R. Jackson ◽  
K. A. Whelan ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Receptor Activity ◽  
Anoikis Resistance ◽  
Human Mammary Epithelial Cells ◽  
Human Mammary Epithelial

scholarly journals Distinct Oncogenic Transcriptomes in Human Mammary Epithelial Cells Infected With Cytomegalovirus

2021 ◽  
Vol 12 ◽  
Author(s):  
Sandy Haidar Ahmad ◽  
Sébastien Pasquereau ◽  
Ranim El Baba ◽  
Zeina Nehme ◽  
Clara Lewandowski ◽  
...  
Keyword(s):  
Breast Cancer ◽  
High Risk ◽  
Epithelial Cells ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Low Risk ◽  
Human Mammary Epithelial Cells ◽  
Mammosphere Formation ◽  
Human Mammary Epithelial

Human cytomegalovirus is being recognized as a potential oncovirus beside its oncomodulation role. We previously isolated two clinical isolates, HCMV-DB (KT959235) and HCMV-BL (MW980585), which in primary human mammary epithelial cells promoted oncogenic molecular pathways, established anchorage-independent growth in vitro, and produced tumorigenicity in mice models, therefore named high-risk oncogenic strains. In contrast, other clinical HCMV strains such as HCMV-FS, KM, and SC did not trigger such traits, therefore named low-risk oncogenic strains. In this study, we compared high-risk oncogenic HCMV-DB and BL strains (high-risk) with low-risk oncogenic strains HCMV-FS, KM, and SC (low-risk) additionally to the prototypic HCMV-TB40/E, knowing that all strains infect HMECs in vitro. Numerous pro-oncogenic features including enhanced expression of oncogenes, cell survival, proliferation, and epithelial-mesenchymal transition genes were observed with HCMV-BL. In vitro, mammosphere formation was observed only in high-risk strains. HCMV-TB40/E showed an intermediate transcriptome landscape with limited mammosphere formation. Since we observed that Ki67 gene expression allows us to discriminate between high and low-risk HCMV strains in vitro, we further tested its expression in vivo. Among HCMV-positive breast cancer biopsies, we only detected high expression of the Ki67 gene in basal tumors which may correspond to the presence of high-risk HCMV strains within tumors. Altogether, the transcriptome of HMECs infected with HCMV clinical isolates displays an “oncogenic gradient” where high-risk strains specifically induce a prooncogenic environment which might participate in breast cancer development.

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