NCI Division of Cancer Biology Junior Investigators Meeting (Abstract): Submission #8

Submission information
Submission Number: 8
Submission ID: 193261
Submission UUID: 0753dfe8-9c63-44d6-a83a-d8ce46a6d249
Submission URI: /dcb/ji-meeting/abstract

Created: Tue, 09/01/2026 - 11:26
Completed: Tue, 09/01/2026 - 11:26
Changed: Tue, 09/01/2026 - 11:26

Remote IP address: 10.208.24.244
Submitted by: Anonymous
Language: English

Is draft: No
First Name Daniel
Middle Initial N
Last Name Phipps
Degree(s) MS
Position/Title/Career Status PhD Candidate
Organization Kashatus Lab/University of Virginia
Organization Address Charlottesville, VA
Email pux6qa@virginia.edu
Abstract Category Use my abstract for team formation only (do not consider it for a presentation)
Abstract Keywords Mitochondrial dynamics, colorectal cancer
Abstract Title Drp1 promotes tumor cell fitness in colorectal cancer through mechanisms independent of mitochondrial fission.
Abstract Colorectal cancer (CRC) ranks as the second leading cause of cancer-related deaths in the United States, and the top cause for cancer-related deaths in patients under 50. Approximately 40% of CRC patients carry an activating mutation in KRAS, a potent driver of oncogenic metabolism and cell replication. Hyperactive KRas signaling is known to promote dynamic structural changes in mitochondrial networks via ERK-mediated activation of the mitochondrial fission GTPase Drp1. Activated Drp1 has been identified as an important player in tumor cell proliferation and survival in RAS-driven disease. However, it remains unclear as to whether the pro-tumorigenic effects of Drp1 are directly attributable to changes in mitochondrial shape, or to presently unknown roles for Drp1 in tumor cell physiology. To address this question, our lab has developed two independent in vitro systems in which we express a fission-incompetent Drp1 in CRC cell lines. Surprisingly, while these cells are devoid of mitochondrial fission, the expression of fission-incompetent Drp1 significantly increases colony formation in comparison to Drp1-null cells. This exciting finding has led us to hypothesize that it is the localization of Drp1 to the outer mitochondrial membrane that induces pro-tumorigenic signaling and metabolism, rather than its canonical function in dividing mitochondria.