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Review
. 2024 Jun 10;15(1):219.
doi: 10.1007/s12672-024-01078-x.

An update on the molecular mechanisms of ZFAS1 as a prognostic, diagnostic, or therapeutic biomarker in cancers

Mahdieh Mehrab Mohseni  1 , Hedyeh Zamani  1 , Mina Momeni  1 , Zeinab Shirvani-Farsani  2
Affiliations
Review

An update on the molecular mechanisms of ZFAS1 as a prognostic, diagnostic, or therapeutic biomarker in cancers

Mahdieh Mehrab Mohseni et al. Discov Oncol. .

Abstract

Zinc finger antisense 1 (ZFAS1), a newly discovered long noncoding RNA, is expressed in various tissues and organs and has been introduced an oncogenic gene in human malignancies. In various cancers, ZFAS1 regulates apoptosis, cell proliferation, the cell cycle, migration, translation, rRNA processing, and spliceosomal snRNP assembly; targets signaling cascades; and interacts with transcription factors via binding to key proteins and miRNAs, with conflicting findings on its effect on these processes. ZFAS1 is elevated in different types of cancer, like colorectal, colon, osteosarcoma, and gastric cancer. Considering the ZFAS1 expression pattern, it also has the potential to be a diagnostic or prognostic marker in various cancers. The current review discusses the mode of action of ZFAS1 in various human cancers and its regulation function related to chemoresistance comprehensively, as well as the potential role of ZFAS1 as an effective and noninvasive cancer-specific biomarker in tumor diagnosis, prognosis, and treatment. We expected that the current review could fill the current scientific gaps in the ZFAS1-related cancer causative mechanisms and improve available biomarkers.

Keywords: Biomarker; Cancer; Chemoresistance; Long noncoding RNA; ZFAS1; miRNA.

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Conflict of interest statement

The authors have no relevant financial or non-financial interests to disclose.

Figures

Fig. 1
Fig. 1
The molecular mechanisms of ZFAS1 in different human cancers. A ZFAS1 blocked GSK-3β via Wnt, which led to β-catenin upregulation. ZFAS1 also upregulated β-catenin via STAT3. B ZFAS1 increased the cell cycle and blocked apoptosis via p53, PARP, and Bax downregulation. ZFAS1 also downregulated PTEN, which blocked PI3K/AKT/mTOR, leading to cell proliferation, invasion, and migration. p53 and PTEN showed a bidirectional positive association. C ZFAS1 interacted with miR‐150 as a ceRNA to over-express ZEB1, MMP14, MMP16, and SP1 to block invasion and metastasis. D ZFAS1 upregulated the mesenchymal markers; MMP2, MMP9, N‐cadherin, Integrin β1, ZEB1, Twist, and Snail, while downregulating the epithelial markers such as E‐cadherin and ZO1, which led to EMT
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