4.7 Article

The critical role of B4GALT4 in promoting microtubule spindle assembly in HCC through the regulation of PLK1 and RHAMM expression

Journal

JOURNAL OF CELLULAR PHYSIOLOGY
Volume 237, Issue 1, Pages 617-636

Publisher

WILEY
DOI: 10.1002/jcp.30531

Keywords

B4GALT family members; B4GALT4; cell microtubule spindle assembly; lumican; PLK1; RHAMM; TGF-beta pathway

Funding

  1. Department of Science and Technology of Jilin Province [20200801066GH]
  2. Education Department of Jilin Province [JJKH20211060KJ]

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The study used bioinformatic methods to explore the expression profiles of B4GALT family in hepatocellular carcinoma (HCC) and found their close association with biological processes such as microtubule spindle assembly, with B4GALT4 playing a crucial role. The research suggests that B4GALT4 is critical for the development of HCC and may provide new strategies for improving patient outcomes.
Beta 1,4-galactosyltransferase (B4GALT)-family glycosyltransferases are involved in multiple biological processes promoting cancer progression, regulating the dynamic network of cancer cell proliferation and apoptosis, and are associated with metastasis. However, their roles in the dysregulation of expressions and functions in hepatocellular carcinoma (HCC) remain unclear. Herein, bioinformatic approaches have been applied to investigate their expression profiles, and to obtain correlations between gene expressions and clinicopathological parameters as well as downstream target genes in HCC. Multiple databases were used to screen the expressions of B4GALT family members in tumor tissues, and to evaluate their prognostic value among HCC patients in different aspects. Results indicated an overall upregulation of B4GALTs' transcription levels in tumor tissues and a strong correlation with poor prognosis. Through Gene Ontology analysis, gene set enrichment analysis, and verification of single-cell RNA sequencing data, we established a connection between the B4GALT family and microtubule spindle assembly, which particularly highlighted the role of B4GALT4 in this phenomenon. B4GALT4 knockdown downregulated the production of lumican, and repressed the expressions of polo-like kinase 1 and RHAMM by regulating the transforming growth factor-beta pathway, thus suggesting that B4GALT4 is a critical promotor for HCC. We believe that these studies will provide valuable insight into the role of B4GALT family members in HCC and lead to the development of new strategies to improve the outcomes for patients with HCC.

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