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

• DOI: 10.3892/ijo.2022.5431
• Publication Date: 2022-09-29T07:22:07Z
• Authors: Qi Zhang; Muhammad Ali; Yang Wang; Qian-Nan Sun; Xiao-Dong Zhu; Dong Tang; Wei Wang; Cang-Yuan Zhang; Hai-Hua Zhou; Dao-Rong Wang
• Keywords: clone (Java method)

The present study aimed to investigate the potential molecular mechanisms by which galectin‑1 (Gal‑1) and glucose‑regulated protein 78 (GRP78) influence development of malignant gastric cancer (GC). Immunohistochemistry western blotting were used map expression location Gal‑1 gene in 80 paraffin‑embedded GC samples, 16 fresh samples surrounding tissues. was overexpressed knocked down using lentiviral vectors human cell lines HGC‑27 AGS. Through use Cell Counting Kit‑8 assay, clone formation wound healing invasion assay tumor xenograft, possible biological roles further evaluated. downstream interacting proteins predicted BioGRID database, GRP78 chosen for investigation. Immunofluorescence labeling Co‑IP confirm connection. statistical tests utilized two‑tailed paired Student's t‑test, χ2 test, Kaplan‑Meier Cox regression analysis, Spearman's rank correlation coefficients. In GC, is extensively expressed has interact with GRP78. Poor prognosis linked high levels patients GC. According functional study, knockdown prevented cells from thriving pushed expression, aided proliferation, migration overexpression additionally subcutaneous xenograft tumors. mechanistic investigation proved that interacted, accelerating course silencing had an inhibitory effect on proliferation removed ectopic whereas stimulating effects AGS inhibited knockdown. conclusion, interacts facilitate advancement Gal‑1/GRP78 axis supported data as a treatment target.