Myc-associated zinc finger protein drives colorectal cancer metastasis through activating ubiquitin like with ring finger protein one.
[BACKGROUND] Colorectal cancer (CRC) is one of the most common causes of cancer mortality worldwide.
APA
Mao HQ, Yu FC, et al. (2025). Myc-associated zinc finger protein drives colorectal cancer metastasis through activating ubiquitin like with ring finger protein one.. World journal of gastrointestinal oncology, 17(11), 109481. https://doi.org/10.4251/wjgo.v17.i11.109481
MLA
Mao HQ, et al.. "Myc-associated zinc finger protein drives colorectal cancer metastasis through activating ubiquitin like with ring finger protein one.." World journal of gastrointestinal oncology, vol. 17, no. 11, 2025, pp. 109481.
PMID
41281490
Abstract
[BACKGROUND] Colorectal cancer (CRC) is one of the most common causes of cancer mortality worldwide. The transcription factor Myc-associated zinc finger protein (MAZ) has been implicated in cancer progression. However, its precise function and mechanisms in CRC remain unclear.
[AIM] To investigate the role and mechanism of the MAZ/ubiquitin-like with PHD and RING finger domains 1 (UHRF1)/esophageal cancer-related gene 4 (ECRG4) axis in CRC metastasis.
[METHODS] Western blot, quantitative reverse transcription polymerase chain reaction (PCR) and transwell were performed to evaluate the impact of MAZ knockdown on CRC cell migration and invasion. A xenograft tumor metastasis model was established by injecting MAZ-deficient CRC cells into nude mice to assess metastatic potential. Dual-luciferase reporter assay was performed to determine the role of MAZ and its downstream target, UHRF1. Chromatin immunoprecipitation-quantitative PCR and methylation-specific PCR were used to analyze whether UHRF1 regulated ECRG4 through DNA methylation.
[RESULTS] MAZ was highly upregulated in CRC cells and promoted CRC migration, invasion, epithelial-mesenchymal transition (EMT) and metastasis. Mechanistically, MAZ transcriptionally activated UHRF1, which in turn led to DNA methylation of ECRG4. Knockdown of MAZ suppressed CRC migration and invasion was reversed by overexpression of UHRF1. Loss of UHRF1 upregulated ECRG4, inhibited EMT, and reduced cell migration and invasion. However, simultaneous knockdown of ECRG4 partially reversed these effects.
[CONCLUSION] MAZ promotes CRC cell migration, invasion, and EMT by transcriptionally activating UHRF1, which downregulates ECRG4 through DNA methylation.
[AIM] To investigate the role and mechanism of the MAZ/ubiquitin-like with PHD and RING finger domains 1 (UHRF1)/esophageal cancer-related gene 4 (ECRG4) axis in CRC metastasis.
[METHODS] Western blot, quantitative reverse transcription polymerase chain reaction (PCR) and transwell were performed to evaluate the impact of MAZ knockdown on CRC cell migration and invasion. A xenograft tumor metastasis model was established by injecting MAZ-deficient CRC cells into nude mice to assess metastatic potential. Dual-luciferase reporter assay was performed to determine the role of MAZ and its downstream target, UHRF1. Chromatin immunoprecipitation-quantitative PCR and methylation-specific PCR were used to analyze whether UHRF1 regulated ECRG4 through DNA methylation.
[RESULTS] MAZ was highly upregulated in CRC cells and promoted CRC migration, invasion, epithelial-mesenchymal transition (EMT) and metastasis. Mechanistically, MAZ transcriptionally activated UHRF1, which in turn led to DNA methylation of ECRG4. Knockdown of MAZ suppressed CRC migration and invasion was reversed by overexpression of UHRF1. Loss of UHRF1 upregulated ECRG4, inhibited EMT, and reduced cell migration and invasion. However, simultaneous knockdown of ECRG4 partially reversed these effects.
[CONCLUSION] MAZ promotes CRC cell migration, invasion, and EMT by transcriptionally activating UHRF1, which downregulates ECRG4 through DNA methylation.