MEIS1 and HOXB13 Support Tumor Suppression By Regulating Decorin and Lumican

Session Number

MEDH 53

Advisor(s)

Mathias Morales, Ryan Brown, Donald Vander Griend, University of Illinois Chicago, Department of Pathology

Discipline

Medical and Health Sciences

Start Date

17-4-2025 2:30 PM

End Date

17-4-2025 2:45 PM

Abstract

Prostate cancer is the second leading cause of cancer-related death in American men. While prostate cancer is very treatable, there remains a need for alternative treatments for those who are resistant to androgen based therapies. MEIS1 and HOXB13 regulation is associated with proteoglycans like decorin and lumican to promote a tumor suppressive phenotype. Therefore, this project aims to elucidate how the transcription factors HOXB13 and MEIS1 work together to act as tumor suppressors by regulating DCN and LUM to inhibit prostate cancer growth. To do this, cancer cell lines 22Rv1 were injected into immunocompromised mice to create xenografts. Then, protein and RNA were harvested from the xenograft tumors. The protein was quantified using BCA analyses before running on Western blots and the RNA was quantified through qPCR. When the cell lines were modulated to overexpress MEIS1, there was an abundance of DCN and LUM. However, when HOXB13 was knocked out the DCN and LUM levels dropped. Analysis of protein-protein interaction prediction through HADDOCK suggests MEIS1-HOXB13 interaction near the C-terminus of the MEIS1 protein. Overall, these results shed light on how MEIS1 and HOXB13 work together to modulate decorin and lumican, providing insight on more effective treatments.

Share

COinS
 
Apr 17th, 2:30 PM Apr 17th, 2:45 PM

MEIS1 and HOXB13 Support Tumor Suppression By Regulating Decorin and Lumican

Prostate cancer is the second leading cause of cancer-related death in American men. While prostate cancer is very treatable, there remains a need for alternative treatments for those who are resistant to androgen based therapies. MEIS1 and HOXB13 regulation is associated with proteoglycans like decorin and lumican to promote a tumor suppressive phenotype. Therefore, this project aims to elucidate how the transcription factors HOXB13 and MEIS1 work together to act as tumor suppressors by regulating DCN and LUM to inhibit prostate cancer growth. To do this, cancer cell lines 22Rv1 were injected into immunocompromised mice to create xenografts. Then, protein and RNA were harvested from the xenograft tumors. The protein was quantified using BCA analyses before running on Western blots and the RNA was quantified through qPCR. When the cell lines were modulated to overexpress MEIS1, there was an abundance of DCN and LUM. However, when HOXB13 was knocked out the DCN and LUM levels dropped. Analysis of protein-protein interaction prediction through HADDOCK suggests MEIS1-HOXB13 interaction near the C-terminus of the MEIS1 protein. Overall, these results shed light on how MEIS1 and HOXB13 work together to modulate decorin and lumican, providing insight on more effective treatments.