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Exploring TSGA10 function: A crosstalk or controlling mechanism in the signaling pathway of carcinogenesis?

Taghizadeh-Hesary, Farzad
; 
Ghadyani, Mobina
; 
Kashanchi, Fatah
; 
Behnam, Babak
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Affiliation
Iran University of Medical Sciences; University of Chester; George Mason University; Avicenna Biotech Research
EPub Date
Publication Date
2024-08-31
Submitted Date
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Chester Medical School
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Abstract
Cancer-specific antigens have been a significant area of focus in cancer treatment since their discovery in the mid-twentieth century. Cancer germline antigens are a class of antigens specifically overexpressed in germline tissues and cancer cells. Among these, TSGA10 (testis-specific gene antigen 10) is of great interest because of its crucial impact on cancer progression. Early studies explored TSGA10 expression in a variety of cancer types. More recent studies revealed that TSGA10 can suppress tumor progression by blocking cancer cell metabolism, angiogenesis, and metastasis. An open question regarding the TSGA10 is why cancer cells must express a protein that prevents their progression. To answer this question, we conducted a comprehensive review to engage the TSGA10 in the context of the current understanding of “malignant transformation”. This review demonstrated that TSGA10 expression level in cancer cells depends on the cancer stage across malignant transformation. In addition, we evaluated how TSGA10 expression can prevent the “cancer hallmarks”. Given this information, TSGA10 can be of great interest in developing effective targeted anti-cancer therapies.
Citation
Taghizadeh-Hesary, F., Ghadyani, M., Kashanchi, F., & Behnam, B. (2024). Exploring TSGA10 function: A crosstalk or controlling mechanism in the signaling pathway of carcinogenesis? Cancers, 16(17), article-number 3044. https://doi.org/10.3390/cancers16173044
Publisher
MDPI
Journal
Cancers
Research Unit
URI
http://hdl.handle.net/10034/628986
DOI
10.3390/cancers16173044
PubMed ID
PubMed Central ID
Type
Article
Language
Description
Series/Report no.
ISSN
EISSN
2072-6694
ISBN
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Unfunded
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https://www.mdpi.com/2072-6694/16/17/3044