LGALS1 drives chemoresistance in esophageal squamous cell carcinoma by modulating epithelial-mesenchymal transition and tumor immunity

Figure 7 LGALS1 diminishes esophageal squamous cell carcinoma cell responsiveness to cisplatin treatment. A: LGALS1, Ki67, and Pan-keratin expression levels in esophageal squamous cell carcinoma specimens compared with adjacent normal esophageal tissue samples; B: Assessment of LGALS1 expression changes under cisplatin administration utilizing quantitative real-time pathological complete remission methodology; C: Evaluation of LGALS1 protein levels following cisplatin exposure as determined by western blot analysis; D: The influence of LGALS1 expression on the cell cycle was analyzed by flow cytometry; E: Clone formation assay examined the influence of LGALS1 expression on cell proliferation; F: Cholecystokinin-8 examined the influence of LGALS1 expression on tumor cell viability under cisplatin treatment; G: The influence of LGALS1 expression on tumor cell apoptosis was ascertained by flow cytometry with cisplatin treatment; H: The phosphorylation levels of the DNA repair-related proteins ATR, CDC25A, Chk1, and p53 were measured by western blot; I: The expression of epithelial-mesenchymal transition and apoptosis-related proteins beta-catenin, E-cadherin, Vimentin, and Bcl2 and BAX was measured by western blot; J: Crystal violet staining was utilized to detect LGALS1 expression on tumor cell proliferation by cisplatin treatment with a concentration gradient. ^aP < 0.05, ^bP < 0.01, NS: Not significant. ESCC: Esophageal squamous cell carcinoma.