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Related Experiment Video

Updated: May 27, 2025

A Genetically Engineered Mouse Model of Sporadic Colorectal Cancer

A Genetically Engineered Mouse Model of Sporadic Colorectal Cancer

Published on: July 6, 2017

METTL1 Enhances RRP9 mRNA Stability Through m7G Modification to Drive Colorectal Tumorigenesis.

Nan Li¹, Ying Jing¹, Long Xu¹

¹Department of Gastroenterology, Jilin Province People's Hospital, Changchun, China.

Molecular Carcinogenesis

|February 17, 2025

Summary

This summary is machine-generated.

METTL1 promotes colorectal cancer (CRC) growth and metastasis by stabilizing RRP9 mRNA through N(7)-methylguanosine (m7G) methylation. Targeting METTL1 and RRP9 offers new therapeutic strategies for CRC.

Keywords:

METTL1 RRP9 colorectal cancer m7G methylation tumorigenesis

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Area of Science:

Molecular Biology
Oncology

Background:

METTL1 is an RNA methyltransferase involved in human tumorigenesis.
Its role in colorectal cancer (CRC) development requires further elucidation.

Purpose of the Study:

To investigate the activity and molecular mechanisms of METTL1 in CRC.
To determine the relationship between METTL1, RRP9, and CRC progression.

Main Methods:

Quantitative PCR, immunoblotting, and immunohistochemistry for gene and protein expression.
In vitro assays (sphere formation, transwell, MTT, wound healing) for cell function.
MeRIP and Actinomycin D treatment to assess mRNA methylation and stability.
In vivo subcutaneous xenograft models.

Main Results:

METTL1 is highly expressed in CRC tumors and cell lines.
METTL1 depletion suppressed CRC cell proliferation, invasion, migration, and sphere formation.
METTL1 positively correlated with RRP9 expression, promoting RRP9 mRNA stability via m7G methylation.
METTL1 regulates PI3K/AKT signaling through RRP9, impacting CRC phenotypes and tumor growth.

Conclusions:

METTL1 acts as a crucial protumorigenic factor in CRC by driving growth, metastasis, and stemness via RRP9.
METTL1-RRP9 axis presents a potential therapeutic target for colorectal cancer treatment.