DNA Methylation-Regulated FAM107A Affects Colorectal Carcinogenesis by Inhibiting FOXM1.
OpenAlex 토픽 ·
FOXO transcription factor regulation
Pancreatic function and diabetes
Signaling Pathways in Disease
[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 associa
APA
Yue Liu, Jinwei Sun, et al. (2026). DNA Methylation-Regulated FAM107A Affects Colorectal Carcinogenesis by Inhibiting FOXM1.. Journal of investigative surgery : the official journal of the Academy of Surgical Research, 39(1), 2633933. https://doi.org/10.1080/08941939.2026.2633933
MLA
Yue Liu, et al.. "DNA Methylation-Regulated FAM107A Affects Colorectal Carcinogenesis by Inhibiting FOXM1.." Journal of investigative surgery : the official journal of the Academy of Surgical Research, vol. 39, no. 1, 2026, pp. 2633933.
PMID
41846456
Abstract
[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 ( < .001). Furthermore, FAM107A overexpression induced apoptosis ( < .001) and cycle arrest in CRC cells. The direct binding of DNMT1 with FAM107A promoter was demonstrated and DNMT1 silencing enhanced FAM107A expression ( < .001). In addition, FOXM1 overexpression stimulated cell proliferation ( < .05, < .001) while suppressing cell apoptosis ( < .01) , and promoted tumor growth ( < .01, < .001) in a Caco-2 cell subcutaneous nude model , which was reversed by FAM107A up-regulation ( < .05, < .01, < .001).
[DISCUSSION] These results hypothesize that the occurrence and development of CRC are mainly mediated by the DNMT1/FAM107A/FOXM1 axis.
[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 ( < .001). Furthermore, FAM107A overexpression induced apoptosis ( < .001) and cycle arrest in CRC cells. The direct binding of DNMT1 with FAM107A promoter was demonstrated and DNMT1 silencing enhanced FAM107A expression ( < .001). In addition, FOXM1 overexpression stimulated cell proliferation ( < .05, < .001) while suppressing cell apoptosis ( < .01) , and promoted tumor growth ( < .01, < .001) in a Caco-2 cell subcutaneous nude model , which was reversed by FAM107A up-regulation ( < .05, < .01, < .001).
[DISCUSSION] These results hypothesize that the occurrence and development of CRC are mainly mediated by the DNMT1/FAM107A/FOXM1 axis.
MeSH Terms
Humans; Colorectal Neoplasms; Forkhead Box Protein M1; DNA Methylation; Cell Proliferation; Apoptosis; Gene Expression Regulation, Neoplastic; DNA (Cytosine-5-)-Methyltransferase 1; Carcinogenesis; Animals; Promoter Regions, Genetic; Caco-2 Cells; Mice; Mice, Nude; Cell Line, Tumor
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