Galectin-1 binds GRP78 to promote the proliferation and metastasis of gastric cancer

The present study aimed to investigate the potential molecular mechanisms by which galectin-1 (Gal-1) and glucose-regulated protein 78 (GRP78) influence the development of malignant gastric cancer (GC). Immunohistochemistry and western blotting were used to map the expression and location of the Gal-1 gene in the 80 paraffin-embedded GC samples, 16 fresh samples and surrounding tissues. Gal-1 was overexpressed and knocked down using lentiviral vectors in the human GC cell lines HGC-27 and AGS. Through the use of the Cell Counting Kit-8 assay, clone formation assay, wound healing assay, invasion assay and tumor xenograft, the possible biological roles of Gal-1 were further evaluated. The downstream interacting proteins were predicted by the BioGRID database, and GRP78 was chosen for further investigation. Immunofluorescence labeling and Co-IP were used to confirm the connection. The statistical tests utilized were the two-tailed paired Student's t-test, χ(2) test, Kaplan-Meier and Cox regression analysis, and Spearman's rank correlation coefficients. In GC, Gal-1 is extensively expressed and has the potential to interact with GRP78. Poor prognosis is linked to high levels of GRP78 and Gal-1 expression in patients with GC. According to the functional study, Gal-1 knockdown prevented cells from thriving and pushed Gal-1 expression, which aided in the proliferation, migration and invasion of GC. Gal-1 overexpression additionally aided the development of subcutaneous xenograft tumors. The mechanistic investigation proved that GRP78 and Gal-1 interacted, accelerating the course of GC. Gal-1 silencing had an inhibitory effect on the proliferation of HGC-27 cells that was removed by ectopic GRP78 expression, whereas the stimulating effects of Gal-1 overexpression in AGS cells were inhibited by GRP78 knockdown. In conclusion, Gal-1 interacts with GRP78 to facilitate the advancement of GC. The Gal-1/GRP78 axis is supported by the functional data of the present study as a possible GC treatment target.