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MASTL Kinase in DNA Repair and Treatment Resistance in Oral Squamous Cell Carcinoma

Award Number: F31DE035010
ORGANIZATION: NATIONAL INSTITUTE OF DENTAL AND CRANIOFACIAL RESEARCH
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 04/08/2026
PERIOD OF PERFORMANCE END DATE: 04/07/2028

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MASTL Kinase in DNA Repair and Treatment Resistance in Oral Squamous Cell Carcinoma - MASTL Kinase in DNA Repair and Treatment Resistance in Oral Squamous Cell Carcinoma Abstract Microtubule Associated Serine Threonine kinase-Like (MASTL) has been shown to promote mitotic progression by suppressing protein phosphatase 2A coupled with targeting subunit B55 (PP2A/B55). Interestingly, MASTL is commonly upregulated in human cancer. In oral squamous cell carcinoma (OSCC), MASTL expression is associated with cancer progression, tumor recurrence, and adverse patient survival. Upregulation of MASTL renders OSCC cells resistant to DNA damage treatments, attenuating post-treatment cell death while promoting cell survival and proliferation. Depletion or inhibition of MASTL significantly enhanced the tumor response to cisplatin in OSCC mouse models. These findings prompt us to hypothesize that MASTL is a potentially effective drug target for OSCC therapy, especially in combination with existing chemoradiation which eliminates cancer cells via induction of DNA damage. However, the precise role of MASTL in mediating DNA damage resistance is still largely unclear; specific strategies to target MASTL kinase in cancer are lacking, representing two major hurdles to the clinical development of MASTL targeting. Our preliminary studies unveiled novel functions of MASTL in DNA repair. MASTL promotes, and B55 suppresses the repair of DNA interstrand crosslinking (ICL) caused by cisplatin. Our data also implicated the MASTL-B55 module in DNA double strand break (DSB) repair via homologous recombination (HR). In Aim 1, we will further investigate these new functions of MASTL, in the context of Fanconi anemia gene pathway that mediates ICL repair and cisplatin resistance, and Rad51- dependent HR that is of strong clinical relevance to treatment responses to chemoradiation and inhibition of poly (ADP-ribose) polymerase (PARP). In Aim 2, we will explore a novel strategy to target MASTL kinase by disrupting its C-terminal domain. This idea, supported by our preliminary data, may guide the development of new and highly selective therapeutic tools for MASTL targeting. Together, our studies will lead to new mechanistic understanding of MASTL-PP2A/B55 in DNA repair and propel the development of new therapeutic strategies to overcome treatment resistance in OSCC.


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 = $42,358 )
2026	2026	UNIVERSITY OF NORTH CAROLINA AT CHAPEL HILL	104 AIRPORT DR STE 2200	CHAPEL HILL	NC	27599	ORANGE	USA	Oral Diseases and Disorders Research	000	1	4/7/2026	NEW	$42,358
2026	2026	UNIVERSITY OF NORTH CAROLINA AT CHAPEL HILL	104 AIRPORT DR STE 2200	CHAPEL HILL	NC	27599	ORANGE	USA	Oral Diseases and Disorders Research	001	1	4/7/2026	NEW	$0
														Subtotal = $42,358

Grand Total All Awards = $42,358

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MASTL Kinase in DNA Repair and Treatment Resistance in Oral Squamous Cell Carcinoma

Award Number: F31DE035010

ORGANIZATION: NATIONAL INSTITUTE OF DENTAL AND CRANIOFACIAL RESEARCH

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 04/08/2026

PERIOD OF PERFORMANCE END DATE: 04/07/2028

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