Mechanisms of GPM6A in Malignant Tumors

IF 1.5 Q4 ONCOLOGY Cancer reports Pub Date : 2025-02-17 DOI:10.1002/cnr2.70137
Bei Huang, Xihong Li
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引用次数: 0

Abstract

Background

Glycoprotein M6A (GPM6A) encodes a transmembrane protein, expressing in large quantities on the cell surface of central nervous system (CNS) neurons. GPM6A acts importantly in neurodevelopment by modulating neuronal differentiation, migration, axon growth, synaptogenesis, and spine formation, but its role in malignancy remains controversial and requires further research. This article reviewed the mechanisms of GPM6A in colorectal cancer, liver cancer, lung cancer, glioblastoma, and other malignant tumors, and made a “one-stop” summary of the relevant mechanisms.

Recent Findings

Researches have indicated that GPM6A is related to malignant tumors. It affects epithelial-mesenchymal transition and induces the formation of filopodia, participating in the adhesion, migration, and metastasis of cancer cells. Its role in malignant tumors remains controversial, however. On the one hand, GPM6A may have carcinogenic properties and is related to poor prognosis of malignant tumors. It is highly expressed in lymphoblastic leukemia and is a potential oncogene. It also shows carcinogenic properties in colorectal cancer, glioblastoma, gonadotroph adenomas and so on. On the other hand, the expression of GPM6A decreases in lung adenocarcinoma, liver cancer, thyroid cancer, and so forth as the tumor progresses, and it can inhibit the progression of malignant tumors by inhibiting some signaling pathways, suggesting that it may be a tumor suppressor gene.

Conclusion

Carcinogenic or tumor suppressive? Although the biological function of GPM6A in the development of malignant tumors is still unclear, according to the current research progress, it is still expected to become an effective molecular marker for predicting tumor occurrence, metastasis and prognosis, as well as a new target for diagnosis and treatment.

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来源期刊
Cancer reports
Cancer reports Medicine-Oncology
CiteScore
2.70
自引率
5.90%
发文量
160
审稿时长
17 weeks
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