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Defining the tumor suppressive mechanism of the kinase STK25

Award Number: F31CA278588
ORGANIZATION: NATIONAL CANCER INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 01/17/2024
PERIOD OF PERFORMANCE END DATE: 01/15/2026
AWARD TERMINATION DATE: 03/27/2026

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Defining the tumor suppressive mechanism of the kinase STK25 - Abstract The maintenance of cellular and tissue homeostasis relies on the tight regulation of cell growth and proliferation. This regulation is predominantly controlled by two evolutionarily conserved pathways: the mammalian Target of Rapamycin (mTOR) pathway and the Hippo pathway. Dysregulation of both the mTOR and Hippo pathways promotes aberrant cell proliferation, tissue overgrowth and tumor development. Elucidating how the mTOR and Hippo signaling pathways coordinate their activities is therefore a vitally important, yet poorly understood, area of cell cancer biology. Our lab previously demonstrated that STK25, a serine/threonine kinase, functions as an upstream activator of Hippo signaling to limit cell growth. Using unbiased approaches, we have now generated strong preliminary data suggesting that the STK25 kinase also functions to impair mTORC1 signaling. We have found that that genetic depletion of STK25 leads to both mTORC1 pathway activation and Hippo pathway inactivation. These data suggest that STK25 may play a critical role in regulating cell proliferation and tumor suppression by coordinating the activities of both the mTORC1 and Hippo signaling pathways. However, the mechanism by which STK25 regulates mTORC1 is unknown. In this proposal, we hypothesize that STK25 directly regulates and phosphorylates key regulatory components of the mTORC1 signaling pathway, ultimately attenuating mTOR signaling. Further, our preliminary studies of STK25 knockout in mice demonstrate that conditional depletion of STK25 is sufficient to induce tumorigenesis, which is congruent with bioinformatic evidence that STK25 is significantly focally deleted in a variety of human cancers. Combining this with our in vitro findings, we also hypothesize that STK25 deficient tumors are dependent on YAP/TAZ and/or mTORC1 activity for growth and survival. These hypotheses will be tested in two specific aims. In Aim 1, we will use cell biological and biochemical approaches to mechanistically define the role of STK25 kinase in regulating mTORC1 activity by characterizing its direct phosphorylated substrates. In Aim 2, we will use a conditional STK25 knockout mouse that we have already generated to determine if STK25 loss facilitates tumorigenesis through increased YAP/TAZ and/or mTORC1 activity. Successful completion of these aims will advance our understanding of mTORC1 and Hippo signaling, and reveal significant new insights into the underlying mechanisms driving tumor development. Moreover, the proposed training plan will greatly enhance my repertoire of skills in microscopy and imaging techniques, molecular cell biology, mouse cancer studies and liquid chromatography mass spectrometry (LC-MS/MS) analysis. Altogether, this will facilitate the development of my scientific expertise in the fields of mTOR and Hippo signaling in cancer biology required for success as an independent scientist.


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: 2026 ( Subtotal = -$2,549 )
2026	2025	TRUSTEES OF BOSTON UNIVERSITY	85 EAST NEWTON ST # M-921	BOSTON	MA	02118	SUFFOLK	USA	Cancer Research Manpower	000	2	3/27/2026	TERMINATION	-$2,549
														Subtotal = -$2,549

Issue Date FY: 2025 ( Subtotal = $49,538 )
2025	2025	TRUSTEES OF BOSTON UNIVERSITY	85 EAST NEWTON ST # M-921	BOSTON	MA	02118	SUFFOLK	USA	Cancer Research Manpower	001	2	5/22/2025	NON-COMPETING CONTINUATION	$564
2025	2025	TRUSTEES OF BOSTON UNIVERSITY	85 EAST NEWTON ST # M-921	BOSTON	MA	02118	SUFFOLK	USA	Cancer Research Manpower	000	2	1/10/2025	NON-COMPETING CONTINUATION	$48,974
														Subtotal = $49,538

Issue Date FY: 2024 ( Subtotal = $48,974 )
2024	2024	TRUSTEES OF BOSTON UNIVERSITY	85 EAST NEWTON ST # M-921	BOSTON	MA	02118	SUFFOLK	USA	Cancer Research Manpower	001	1	12/29/2023	NEW	$0
2024	2024	TRUSTEES OF BOSTON UNIVERSITY	85 EAST NEWTON ST # M-921	BOSTON	MA	02118	SUFFOLK	USA	Cancer Research Manpower	000	1	12/29/2023	NEW	$47,694
2024	2024	TRUSTEES OF BOSTON UNIVERSITY	85 EAST NEWTON ST # M-921	BOSTON	MA	02118	SUFFOLK	USA	Cancer Research Manpower	002	1	5/7/2024	NEW	$1,280
														Subtotal = $48,974

Grand Total All Awards = $95,963

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Defining the tumor suppressive mechanism of the kinase STK25

Award Number: F31CA278588

ORGANIZATION: NATIONAL CANCER INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 01/17/2024

PERIOD OF PERFORMANCE END DATE: 01/15/2026

AWARD TERMINATION DATE: 03/27/2026

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