The role of ASXL1 mutations and ASXL1 CircRNAs in cancer

Abstract

Background

Mutations in the Additional Sex Combs Like 1 (ASXL1) gene were first reported in myelodysplastic syndromes. Recent studies have clarified the relationship between ASXL1 mutations and the development of cancers.

Objective

This study aims to review the roles of ASXL1 and ASXL1 CircRNAs, such as epigenetic regulation, chromatin modification, and transcription factor function in malignancies.

Method

This study is a review of articles related to the role of ASXL1 and ASXL1 CircRNAs in malignancies, retrieved from PubMed and Scopus.

Results

ASXL1 plays a role in malignancies and is also related to poor overall survival and cancer metastasis. ASXL1 encodes conserved and abundant Circular RNAs (circRNAs) that act as post-transcriptional regulators, regulating tumorigenesis and progression in cancer. ASXL1 circRNA was identified in the top 10% of differentially expressed circRNAs in clinically relevant tissues. Additionally, the role of ASXL1 gene circRNAs in cancer development is reviewed in this study.

Conclusion

ASXL1 and ASXL1circRNA have dual functions in combination with different proteins, being involved in both transcriptional activation and repression in a context-dependent manner. Moreover, studies indicate these genes play an important role in epithelial-mesenchymal transition (EMT) and metastasis. Ongoing research is aimed at determining this gene family’s function in biological events.

Keywords:

• ASXL1
• CircRNA
• cancer

Acknowledgments

Figures were created with BioRender.com

Consent for publication

All authors have approved the manuscript and agree with its submission.

Authors’ contributions

Rezvan Esmaeili: corresponding author, conceptualization, writing, critical review and editing. Narges Jafarbeik Iravani: literature search, writing, and original draft preparation. Sara Kolahdozan: literature search and information collection.

Disclosure statement

No potential conflict of interest was reported by the authors.

Additional information

Funding

This work is supported by grant No.3067-2 from ACECR.