Year: 2018
Type: dissertation
Abstract: Cancer initiating cells (CICs) are known for their ability to self-renew while simultaneously giving rise to the tumor bulk. Attention has been given to their unique metabolic mechanisms to ensure their survival. Mitochondrial fission, regulated by dynamin-related protein 1 (DRP1), is upregulated in many cancers, and is required for the CIC fraction to maintain their stemness. Inhibiting DRP1 activity with pharmacological agent mitochondrial division inhibitor 1 (mdivi-1) results in decreased cell growth, viability, and importantly, tumorsphere formation. We hypothesize that colon cancer initiating cells (CCICs) are more dependent on DRP1 than non-colon cancer initiating cells (non-CCICs), and treatment of cultures with mdivi-1 will reduce proliferation and survival due to decreased DRP1 function. We find CCICs to express lower activated DRP1, yet their rate of proliferation decreased at a higher rate to the non-CCICs, while having a less viable population. We provide support that mdivi-1 treatment can compromise CCIC activity.
Source: TSpace (University of Toronto)
Author: Sheila Wang
Language: English
Topic: Cancer Cells and Metastasis
Subfield: Oncology
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W3164991628