Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

C. elegans Germline as Three Distinct Tumor Models

Version 1 : Received: 11 May 2024 / Approved: 12 May 2024 / Online: 13 May 2024 (12:15:25 CEST)

How to cite: Jones, M. E.; Norman, M.; Tiet, A. M.; Lee, J.; Lee, M. H. C. elegans Germline as Three Distinct Tumor Models. Preprints 2024, 2024050777. https://doi.org/10.20944/preprints202405.0777.v1 Jones, M. E.; Norman, M.; Tiet, A. M.; Lee, J.; Lee, M. H. C. elegans Germline as Three Distinct Tumor Models. Preprints 2024, 2024050777. https://doi.org/10.20944/preprints202405.0777.v1

Abstract

Tumor cells display abnormal growth and division, avoiding the natural process of cell death. These cells can be benign (non-cancerous growth) or malignant (cancerous growth). Over the past few decades, numerous in vitro or in vivo tumor models have been employed to understand the molecular mechanisms associated with tumorigenesis in diverse aspects. However, our comprehension of how non-tumor cells transform into tumor cells at molecular and cellular levels remains incomplete. The nematode C. elegans has emerged as an excellent model organism for exploring various phenomena, including tumorigenesis. Although C. elegans does not naturally develop cancer, it serves as a valuable platform for identifying oncogenes and the underlying mechanisms within a live organism. In this review, we describe three distinct germline tumor models in C. elegans, highlighting their associated mechanisms and related regulators. Given the conservation of many of the regulators implicated in C. elegans tumorigenesis, it is proposed that these unique models hold significant potential for enhancing our comprehension of the broader control mechanisms governing tumorigenesis.

Keywords

Tumorigenesis; GLP-1/Notch signaling; RNA-binding proteins; GLD-1; PUF-8; C. elegans germline

Subject

Biology and Life Sciences, Cell and Developmental Biology

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