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Updated: Mar 19, 2026

Continuous Fluorescence-Based Endonuclease-Coupled DNA Methylation Assay to Screen for DNA Methyltransferase Inhibitors
Published on: August 5, 2022
DNA Methylation-Regulated FAM107A Affects Colorectal Carcinogenesis by Inhibiting FOXM1
Yue Liu1, Jinwei Sun1, Yuhua Shi1
1The Yancheng School of Clinical Medicine of Nanjing Medical University, Yancheng Third People's Hospital, Yancheng, Jiangsu, China.
Introduction:
Family with sequence similarity 107 member A (FAM107A) has been reported to inhibit cancer cell proliferation and migration and enhance apoptosis; however, to our knowledge, the association between FAM107A and colorectal cancer (CRC) has not been explored.
Methods:
CCK-8 assay, colony formation, EdU, flow cytometry assays were used to detect the cellular aggressive behaviors. FAM107A promoter methylation was analyzed by bioinformatics tools. The interaction between DNMT1 and FAM107A was explored by RT-qPCR, Western blot and ChIP assay.
Results:
Overexpression of FAM107A inhibited CRC cell proliferation (p < .001). Furthermore, FAM107A overexpression induced apoptosis (p < .001) and cycle arrest in CRC cells. The direct binding of DNMT1 with FAM107A promoter was demonstrated and DNMT1 silencing enhanced FAM107A expression (p < .001). In addition, FOXM1 overexpression stimulated cell proliferation (p < .05, p < .001) while suppressing cell apoptosis (p < .01) in vitro, and promoted tumor growth (p < .01, p < .001) in a Caco-2 cell subcutaneous nude model in vivo, which was reversed by FAM107A up-regulation (p < .05, p < .01, p < .001).
Discussion:
These results hypothesize that the occurrence and development of CRC are mainly mediated by the DNMT1/FAM107A/FOXM1 axis.
Insights
Family with sequence similarity 107 member A (FAM107A) inhibits colorectal cancer (CRC) cell growth and promotes apoptosis. The DNMT1/FAM107A/FOXM1 axis is identified as a key regulator in CRC development.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Family with sequence similarity 107 member A (FAM107A) is known to suppress cancer progression.
- The role of FAM107A in colorectal cancer (CRC) has not been previously investigated.
Purpose of the Study:
- To explore the association between FAM107A and colorectal cancer (CRC).
- To investigate the regulatory mechanism of FAM107A in CRC progression.
Main Methods:
- Cellular aggressive behaviors were assessed using CCK-8, colony formation, EdU, and flow cytometry assays.
- FAM107A promoter methylation and the interaction between DNMT1 and FAM107A were analyzed using bioinformatics, RT-qPCR, Western blot, and ChIP assays.
Main Results:
- FAM107A overexpression significantly inhibited CRC cell proliferation, induced apoptosis, and caused cell cycle arrest.
- DNMT1 was found to directly bind to the FAM107A promoter, and DNMT1 silencing enhanced FAM107A expression.
- FOXM1 overexpression promoted CRC cell proliferation and tumor growth, which was reversed by FAM107A upregulation.
Conclusions:
- The DNMT1/FAM107A/FOXM1 axis plays a crucial role in the occurrence and development of colorectal cancer (CRC).
- FAM107A acts as a tumor suppressor in CRC, potentially through its interaction with DNMT1 and FOXM1.
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