Recent advances of GOLM1 in hepatocellular carcinoma

Abstract

Hepatocellular carcinoma (HCC) is one of the most common liver malignancies and is a leading cause of cancer-related deaths. Most HCC patients are diagnosed at an advanced stage and current treatments show poor therapeutic efficacy. It is particularly urgent to explore early diagnosis methods and effective treatments of HCC. There are a growing number of studies that show GOLM1 is one of the most promising markers for early diagnosis and prognosis of HCC. It is also involved in immune regulation, activation and degradation of intracellular signaling factors and promotion of epithelial–mesenchymal transition. GOLM1 can promote HCC progression and metastasis. The understanding of the GOLM1 regulation mechanism may provide new ideas for the diagnosis, monitoring and treatment of HCC.

Keywords::

• diagnosis
• GOLM1
• hepatocellular carcinoma
• immune system
• prognosis

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Erratum

Author contributions

J Yan and B Zhou consulted the literature, analyzed the data, summarized and wrote the manuscript. H Li and L Guo analyzed the literature data and revised the manuscript. Q Ye supervised the design of this review, analyzed the literature data, made a summary and revised the manuscript. All authors approved the final version of the manuscript.

Financial & competing interests disclosure

This work was supported in part by the Program of Shanghai Subject Chief Scientist (no. 16XD1400800) and the National Natural Science Foundation of China (no. 81572301, 81502487, 81802893 and 81871924). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Additional information

Funding

This work was supported in part by the Program of Shanghai Subject Chief Scientist (no. 16XD1400800) and the National Natural Science Foundation of China (no. 81572301, 81502487, 81802893 and 81871924). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.