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Updated: Apr 12, 2026
A Method for Measuring RNA N6-methyladenosine Modifications in Cells and Tissues
Published on: December 5, 2016
FTO-mediated m6A demethylation inhibits bladder cancer progression via decreasing EMG1 and reducing ribosome
Kun Yao1, Long Wang1, Jinrong Wang1
1Department of Urology, The Third Xiangya Hospital, Central South University, Changsha, Hunan, 410013, China.
Abstract:
Bladder cancer (BLCA) is one of the most common urological malignancies, entailing significant morbidity and mortality rates. A comprehensive understanding of the mechanisms driving bladder cancer initiation and development is required to devise improved treatment regimens. N6-methyladenosine (m6A) is the most prevalent internal RNA modification reported to regulate cancer metastasis. Here, the function of fat mass and obesity-associated protein (FTO), an m6A demethylase, was studied in bladder cancer by overexpressing or knocking down FTO, and the underlying mechanism of FTO in BLCA was explored using machine learning analysis, in vitro, and in vivo experiments. The FTO expression has been proven to be downregulated within bladder cancer, and it could exert a tumor-suppressive effect. Moreover, Gain- and loss-of-function experiments showed that FTO downregulation enhanced the proliferation, migration, and invasion of bladder cancer cells. Mechanistic studies revealed that FTO decreased EMG1 expression by demethylating EMG1 and reducing ribosome biosynthesis, thereby promoting bladder cancer cell proliferation, migration, and invasion and repressing tumor growth in vivo. This study has demonstrated the anti-tumor effect of FTO on bladder cancer development, making it a promising therapeutic target.
Insights
Fat mass and obesity-associated protein (FTO) acts as a tumor suppressor in bladder cancer (BLCA). FTO downregulation promotes cancer cell growth and invasion, indicating its potential as a therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Epigenetics
Background:
- Bladder cancer (BLCA) presents a significant global health challenge, necessitating deeper understanding of its developmental mechanisms.
- N6-methyladenosine (m6A) RNA modification is implicated in cancer progression and metastasis.
- Fat mass and obesity-associated protein (FTO) is an m6A demethylase with a known role in various cancers.
Purpose of the Study:
- To investigate the functional role of FTO in bladder cancer (BLCA) progression.
- To elucidate the underlying molecular mechanisms by which FTO influences BLCA.
- To evaluate FTO as a potential therapeutic target for bladder cancer.
Main Methods:
- Overexpression and knockdown of FTO in BLCA cell lines.
- Machine learning analysis to explore FTO's mechanism.
- In vitro and in vivo experiments to assess FTO's functional impact.
- Analysis of FTO's effect on EMG1 expression and ribosome biosynthesis.
Main Results:
- FTO expression is downregulated in bladder cancer tissues, suggesting a tumor-suppressive role.
- FTO knockdown enhanced BLCA cell proliferation, migration, and invasion.
- FTO demethylates EMG1, reducing ribosome biosynthesis and consequently promoting tumor growth.
- FTO demonstrated an anti-tumor effect in vivo.
Conclusions:
- FTO exhibits significant anti-tumor activity in bladder cancer.
- FTO's mechanism involves regulating EMG1 and ribosome biosynthesis.
- FTO represents a promising therapeutic target for bladder cancer treatment.
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