School of Science Division of Life Science 36 Targeting Mitotic Regulators in Cancer Cells for Potential Treatment Supervisor: POON Randy Yat Choi / LIFS Student: LI Haiyue / BCB Course: UROP 1000, Summer Reactive oxygen species (ROS) are known to play an essential role in maintaining cellular activities, while a ROS disorder could usually cause various diseases in human especially cancer (Nakamura & Takada, 2021). An increased oxidative stress promotes cell proliferation through remodeling the signaling and metabolism pathways, so therefore it is known as a hallmark of cancer. In previous experiments in our laboratory, knocking out a key mitochondria redox defense protein Superoxide Dismutase 2 (SOD2) was found to result in abolition of proliferation in HeLa cells (Ning, 2024). I founded that the SOD2-Flag protein in a SOD2knockout cell line was only partially turned off with a 40-hour doxycycline treatment. Together with a double thymidine synchronization and nocodazole treatment to trap cells in mitosis (M phase), most of the SOD2expressing cells underwent apoptosis shortly after entering M. Also, nocodazole was found to promote SOD2-Flag expression. Whether cells with SOD2-Flag gene turned off after longer doxycycline treatment can be trapped in M is still under investigation. While these experiments are still ongoing, this report is based on the experiments that were performed in the last few months and future experimental plans. Targeting Mitotic Regulators in Cancer Cells for Potential Treatment Supervisor: POON Randy Yat Choi / LIFS Student: NASEER Nayab Qureshi / BIBU Course: UROP 1100, Fall Muntjac deer cells show a striking karyotype difference from the non-traditional model organisms. The chromosome-scale genome assemblies for Indian muntjacs, Muntiacus muntjak vaginalis is (2n = 6/7). We analysed the induced tetraploidy from their diploid progenitors by manipulating mitosis and cytokinesis using a sequential drug treatment with Nocodazole (NOC) and Dihydrocytochalasin B (DCB), respectively. The proposed methodology involves arresting Muntjac deer cells in mitosis and subsequently inhibiting cytokinesis. However, current obstacles include the cytotoxic effects observed when applying standard doses of NOC (0.1 µg/mL) and DCB (4 µM). By using optimal concentrations of these agents, we were able to generate tetraploid Muntjac deer cells through the sequential treatment strategy without eliciting cell death. In order to visualise the chromosome assembly, diploid Muntjac deer cells were stained with several different primary antibodies including, γ-Tubulin, Aurora-A and C-NAP 1, allowing us to study genome stability. Implications: These findings could offer critical insights into cell cycle regulation and ploidy manipulation in non-traditional model organisms, contributing to the development of more effective and targeted cancer treatments in the future.
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