MCF-7 breast cancer cells, overexpression of HHLA2, HHLA2 glycosylation
Abstract
Purpose: Since HHLA2 protein is overexpressed in BC tumors and its glycosylation promotes immune system escape and accelerates tumor progression, this paper aimed to investigate whether HHLA2 protein induces its glycosylation and improves the survival and reduces apoptosis of MCF-7 breast cancer cells. This paper hopes that this inquiry will lead to the development of new therapies to control the overexpressed HHLA2 protein in solid tumors, particularly breast cancer, to inhibit breast cancer progression. Methods: Measure glycosylation by mass shift on western blot, measure viability by MTT assay, and apoptosis by Annexin V/PI FACs. Positive control is Taxol, negative control is the blank control group. Possible results: There are four possible outcomes: (1) HHLA2 overexpression promotes self-glycosylation, increases MCF-7 breast cancer cell survival, and reduces apoptosis. (2) HHLA2 overexpression does not promote self-glycosylation but increases MCF-7 breast cancer cell survival and reduces apoptosis. (3) HHLA2 overexpression does not promote self-glycosylation and does not increase MCF-7 breast cancer cell survival, or reduce apoptosis. (4) HHLA2 overexpression promotes self-glycosylation but does not increase MCF-7 breast cancer cell survival and reduce apoptosis. Conclusion: The observed phenomenon will be useful for future immunotherapy against HHLA2 for breast cancer.
