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This galley proof is being listed electronically before publishing the final manuscript (It's not final version).

Non-classical role of Galectin-3 in cancer progression: Translocation to nucleus by carbohydrate-recognition independent manner
Seok-Jun Kim 1,2 (Associate professor), Kyung-Hee Chun 3,4,* (Associate professor)
1Department of Biomedical Science College of Natural Science and 2Department of Life Science & Brain Korea 21 Plus Research Team for Bioactive Control Technology, Chosun University, Gwangju 61452, Republic of Korea,
3Department of Biochemistry & Molecular Biology, Yonsei University College of Medicine and 4Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul, 03722, Republic of Korea
Galectin-3 is a carbohydrate-binding protein and regulates diverse functions, including cell proliferation and differentiation, mRNA splicing, apoptosis induction, immune surveillance and inflammation, cell adhesion, angiogenesis, and cancer-cell metastasis. Galectin-3 is also recommended as a diagnostic or prognostic biomarker of various diseases, including heart disease, kidney disease, and cancer. Galectin-3 exists as a cytosol, is secreted in extracellular spaces on cells, and is also detected in nuclei. It has been found that galectin-3 has different functions in cellular localization: (i) Extracellular galectin-3 mediates cell attachment and detachment. (ii) cytosolic galectin-3 regulates cell survival by blocking the intrinsic apoptotic pathway, and (iii) nuclear galectin-3 supports the ability of the transcriptional factor for target gene expression. In this review, we focused on the role of galectin-3 on translocation from cytosol to nucleus, because it happens in a way independent of carbohydrate recognition and accelerates cancer progression. We also suggested here that intracellular galecin-3 could be a potent therapeutic target in cancer therapy.
Abstract, Accepted Manuscript(in press) [Submitted on January 30, 2020, Accepted on February 19, 2020]
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