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Galectins dysregulation: A way for cancer cells to invade and pervade

MAHMOUD M. ABDELFATTAH1, REHAM HELWA1,2,*

1 Molecular Cancer Biology Group, Zoology Department, Faculty of Science, Ain Shams University, Cairo, Egypt
2 Faculty of Basic Science, King Salman International University, South Sinai, Egypt

* Corresponding Author: REHAM HELWA. Email: email

Oncology Research 2022, 30(3), 129-135. https://doi.org/10.32604/or.2022.026838

Abstract

Galectins are sticky molecules that bind to β-galactoside. Their interactions render them essential players in many cellular processes. The imbalance of galectin expression was reported in many diseases. In cancer, galectins interact with the extracellular matrix, evade the immune system, and potentially have broad interactions with blood components. In the last ten years, since 2010, we did focus on galectin research in different cancer types. Our findings showed an interaction between cancer cells and erythrocytes via galectin-4. Moreover, we found that upregulation of galectins was associated with lymph node metastasis in ovarian cancers. Hence, with this, we shortly review some important aspects of galectins and their potential importance in more profound understanding of cancer progression and the field of cancer biomarkers.

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APA Style
ABDELFATTAH, M.M., HELWA, R. (2022). Galectins dysregulation: A way for cancer cells to invade and pervade. Oncology Research, 30(3), 129-135. https://doi.org/10.32604/or.2022.026838
Vancouver Style
ABDELFATTAH MM, HELWA R. Galectins dysregulation: A way for cancer cells to invade and pervade. Oncol Res. 2022;30(3):129-135 https://doi.org/10.32604/or.2022.026838
IEEE Style
M.M. ABDELFATTAH and R. HELWA, "Galectins dysregulation: A way for cancer cells to invade and pervade," Oncol. Res., vol. 30, no. 3, pp. 129-135. 2022. https://doi.org/10.32604/or.2022.026838



cc This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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