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The role of UbcH7 in male breast cancer

Award Number: R03CA289857
ORGANIZATION: NATIONAL CANCER INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 04/01/2024
PERIOD OF PERFORMANCE END DATE: 03/31/2026

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The role of UbcH7 in male breast cancer - Abstract While breast cancer is one of the most common cancers in women in the U.S., it is extremely rare in men, accounting for less than 1% of all breast cancer cases. Although there are several factors that may increase the risk of developing male breast cancer, the fundamental disease-defining molecular pathway of this rare cancer remains unknown. As a result, male breast cancer has been considered similar to female breast cancer even though accumulating evidence indicates that breast cancers in men may be genetically and epigenetically distinct. Unfortunately, unlike female breast cancer, the lack of model systems hinders the investigation of male breast cancer. The ubiquitin/proteasome system (UPS) plays a critical role in the regulation of protein quality control through protein degradation. Dysregulation of the UPS has been implicated in several diseases, including neurodegenerative disorders and cancer. The UPS is composed of 3 critical enzymes: ubiquitin-activating enzymes (E1), ubiquitin-conjugating enzymes (E2), and ubiquitin ligases (E3). While E3 ligases are often found to be dysregulated in cancer, the pathophysiological significance of the E2 ubiquitin-conjugating enzymes remains elusive. UbcH7 (also known as Ube2l3) is one of the E2 enzymes ubiquitously expressed in various tissues and organs. Our lab has recently discovered that UbcH7 heterozygosity (UbcH7+/) significantly promotes the incidence of male breast cancer in MMTV-Neu mice, a mouse model of HER2+ human breast cancer. Importantly, the loss of one copy of UbcH7 does not have any effects in female breast cancer. To the best of our knowledge, this is the first transgenic mouse model that promotes breast cancer only in males. Based on these results, we hypothesize that UbcH7 plays a unique role in the prevention of male breast cancer by promoting the degradation of an oncoprotein which only influences mammary tumorigenesis in males. The ultimate goal of this project is to identify the “male-specific oncoprotein” in breast cancer. Towards this goal, we will first investigate the pathophysiological conditions of UbcH7+/- male mice, especially focusing on mammary gland development (Aim 1). We will then perform in vivo 2H2O-labeling and mass spectrometry-based proteomics to identify the substrates of UbcH7 in male mammary glands (Aim 2). Furthermore, we also plan to conduct RNA-seq to identify an altered signaling pathway(s) in UbcH7+/- mammary glands. Despite numerous studies on breast cancer, the mechanisms that regulate male breast cancer remain poorly understood. We expect that our studies will place UbcH7 as a novel predisposition gene for the development of male breast cancer, serving as a breakthrough that will open up a new direction of research in this field.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2025 ( Subtotal = $81,001 )
2025	2025	KENT STATE UNIVERSITY	1500 HORNING RD	KENT	OH	44242	PORTAGE	USA	Cancer Biology Research	000	2	3/13/2025	NON-COMPETING CONTINUATION	$81,001
														Subtotal = $81,001

Issue Date FY: 2024 ( Subtotal = $84,433 )
2024	2024	KENT STATE UNIVERSITY	1500 HORNING RD	KENT	OH	44242	PORTAGE	USA	Cancer Biology Research	000	1	4/1/2024	NEW	$84,433
														Subtotal = $84,433

Grand Total All Awards = $165,434

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The role of UbcH7 in male breast cancer

Award Number: R03CA289857

ORGANIZATION: NATIONAL CANCER INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 04/01/2024

PERIOD OF PERFORMANCE END DATE: 03/31/2026

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