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Related Experiment Video

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Long-term Live-cell Imaging to Assess Cell Fate in Response to Paclitaxel

Long-term Live-cell Imaging to Assess Cell Fate in Response to Paclitaxel

Published on: May 14, 2018

Sequential oncogenic mutations influence cell competition.

Koki Kohashi¹, Yusuke Mori¹, Rika Narumi²

¹Department of Molecular Oncology, Kyoto University Graduate School of Medicine, Kyoto, Japan; Division of Molecular Oncology, Institute for Genetic Medicine, Hokkaido University Graduate School of Chemical Sciences and Engineering, Sapporo, Japan.

Current Biology : CB

|July 27, 2021

Summary

This summary is machine-generated.

Sequential oncogenic mutations can alter cell competition dynamics. Ras and Scribble mutations in mammalian cells shift competition, promoting survival of mutated cells and impacting cancer development.

Keywords:

ROS RasV12 Scribble apoptosis cell competition engulfment entosis mTOR mitochondria sequential mutations

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Area of Science:

Cell Biology
Cancer Research
Developmental Biology

Background:

Cell competition eliminates transformed cells during early carcinogenesis.
The role of cell competition in later cancer development with multiple mutations is unclear.

Purpose of the Study:

Investigate cell competition dynamics following consecutive Ras and Scribble mutations.
Determine the mechanisms underlying altered cell competition in cancer development.

Main Methods:

Mammalian cell culture models.
Drosophila epithelial tissue experiments.
Mitochondrial membrane potential and reactive oxygen species (ROS) analysis.
Mechanistic target of rapamycin kinase (mTOR) pathway investigation.

Main Results:

Ras mutation under Scribble-knockdown diminishes apical extrusion of double-mutant cells.
Scribble/Ras cells induce apoptosis and engulfment of surrounding Scribble-knockdown cells.
Enhanced mitochondrial metabolism (membrane potential, ROS) drives these competitive interactions.
mTOR acts downstream of mitochondrial activity in this process.

Conclusions:

Sequential oncogenic mutations reprogram cell competition, enabling mutated cells to become 'winners'.
Mitochondrial metabolism and mTOR signaling are key regulators of this altered competition.
Findings suggest novel therapeutic strategies targeting cell competition in cancer treatment.