Deciphering the role of AMPK-related kinase 5 in human cancer progression and metastasis

Authors

  • Alfredo Bambang Department of Chemistry and Biochemistry, School of Medicine and Health Sciences, Atma Jaya Catholic University of Indonesia, Jakarta, 14440, Indonesia
  • Caroline Tanadi Undergraduate Medical Program, School of Medicine and Health Sciences, Atma Jaya Catholic University of Indonesia, Jakarta 14440, Indonesia
  • Anton Sumarpo Department of Chemistry and Biochemistry, School of Medicine and Health Sciences, Atma Jaya Catholic University of Indonesia, Jakarta, 14440, Indonesia https://orcid.org/0000-0001-5196-4510

DOI:

https://doi.org/10.15419/bmrat.v6i10.568

Keywords:

ARK5, biomarker, cancer, epigenetics, invasion, tumor proliferation

Abstract

Malignancies related mortality is currently growing at an alarming rate. Early detection of cancer is vital in order to improve survival rates of cancer patients, and biomarker detection is regarded as one of the most promising approaches. Recent studies have reported that elevated AMPK-related kinase 5 (ARK5) expression is associated with tumor progression and metastasis in several human malignancies. Several pathways are also influenced by the presence of ARK5, most notably the PI3k-Akt pathway, m-TOR phosphorylation, and several pathways that induce increased tumor invasion activity. Additionally, ARK5 expression are linked to miR-1181 down-regulation, which promotes epithelial mesenchymal transformation in ovarian cancer cells. Furthermore, ARK5 gene transcription is also affected by the interaction of c-MAF and MAFB with both MARE core sequences present in the ARK5 promoter. Based on the current evidences, ARK5 might be the master regulator of cancer progression and metastasis, which could potentially serve as a novel target for cancer therapies.

 

Published

2019-10-24

Issue

Section

Review

How to Cite

Deciphering the role of AMPK-related kinase 5 in human cancer progression and metastasis. (2019). Biomedical Research and Therapy, 6(10), 3396-3404. https://doi.org/10.15419/bmrat.v6i10.568

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