Impact of MFAP5-Overexpressing on Breast Cancer Progression

Publication Date

July 2026

Document Type

Abstract

Start Date

24-7-2026 9:00 AM

End Date

24-7-2026 3:00 PM

Description

Estrogen receptor positive (ER+) breast cancer accounts for 70% of breast cancers, making it the most common subtype of breast cancer. 40% of ER+ breast cancers develop resistance to of endocrine therapy and progress to a more aggressive phenotype. While prior studies suggest alterations to ER expression and activation, to date, the cell-extrinsic mediators of tumor progression remain incompletely understood. Microfibrillar-associated glycoprotein 5 (MFAP5) is a matrix-associated protein linked to tumor invasion, metastasis, and poor prognosis in breast cancer. However, the role of MFAP5 in ER+ breast cancer is not yet defined. To determine the impact of cell-extrinsic mediator MFAP5 on ER+ breast cancer progression and ER signaling, MFAP5 was overexpressed in the ER+ cell line, MCF-7. We validated overexpression of MFAP5 gene and protein (cell lysate and media) expression in MCF-7-MFAP5 OE cell lines compared to MCF-7 vector control. RNA sequencing results demonstrated alterations to mTOR/AKT and TGF-β signaling pathways, with additional changes observed in ER-mediated genes. Further confirmation studies showed a significant decrease in the ER response gene progesterone receptor (PGR) but no change in ER in MFAP5-OE cells compared to vector control cells. Estradiol (E2) treatment increased PGR expression, suggesting ER function remained. Overall, our results demonstrate that MFAP5 enhances expression of genes associated with growth and EMT-related signaling pathways, while suppressing PGR. Together, this suggests the ECM protein MFAP5 as a cell-extrinsic mediator of the ER signaling axis. Future work will expand on this to determine if MFAP5 alters the endocrine response in ER+ breast cancer.

Comments

Mentor: Dr. Matthew Burrow, Tulane University

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Jul 24th, 9:00 AM Jul 24th, 3:00 PM

Impact of MFAP5-Overexpressing on Breast Cancer Progression

Estrogen receptor positive (ER+) breast cancer accounts for 70% of breast cancers, making it the most common subtype of breast cancer. 40% of ER+ breast cancers develop resistance to of endocrine therapy and progress to a more aggressive phenotype. While prior studies suggest alterations to ER expression and activation, to date, the cell-extrinsic mediators of tumor progression remain incompletely understood. Microfibrillar-associated glycoprotein 5 (MFAP5) is a matrix-associated protein linked to tumor invasion, metastasis, and poor prognosis in breast cancer. However, the role of MFAP5 in ER+ breast cancer is not yet defined. To determine the impact of cell-extrinsic mediator MFAP5 on ER+ breast cancer progression and ER signaling, MFAP5 was overexpressed in the ER+ cell line, MCF-7. We validated overexpression of MFAP5 gene and protein (cell lysate and media) expression in MCF-7-MFAP5 OE cell lines compared to MCF-7 vector control. RNA sequencing results demonstrated alterations to mTOR/AKT and TGF-β signaling pathways, with additional changes observed in ER-mediated genes. Further confirmation studies showed a significant decrease in the ER response gene progesterone receptor (PGR) but no change in ER in MFAP5-OE cells compared to vector control cells. Estradiol (E2) treatment increased PGR expression, suggesting ER function remained. Overall, our results demonstrate that MFAP5 enhances expression of genes associated with growth and EMT-related signaling pathways, while suppressing PGR. Together, this suggests the ECM protein MFAP5 as a cell-extrinsic mediator of the ER signaling axis. Future work will expand on this to determine if MFAP5 alters the endocrine response in ER+ breast cancer.