Sulfasalazine inhibits esophageal cancer cell proliferation by mediating ferroptosis.

This study aimed to explore the potential mechanism by which sulfasalazine (SAS) inhibits esophageal cancer cell proliferation. A cell counting kit-8 (CCK-8) assay was used to detect the effect of SAS (0, 1, 2, and 4 mM) on the proliferation of TE-1 cells. Subsequently, TE-1 cells were divided into control group, SAS group, SAS + ferrostatin-1 (ferroptosis inhibitor) group, and SAS + Z-VAD (OH)-FMK (apoptosis inhibitor) group, and cell proliferation was measured using a CCK-8 assay. Real-time quantitative polymerase chain reaction and western blotting were used to determine the expression of solute carrier family member 7 11 (SLC7A11, also called xCT), glutathione peroxidase 4 (GPX4), and acyl-CoA synthase long-chain family member 4 (ACSL4) in TE-1 cells. Measurement of ferroptosis in TE-1 cells was achieved by flow cytometry. Compared with the control group (0 mM SAS), the proliferation of TE-1 cells was significantly inhibited by different concentrations of SAS for different time lengths, and 4 mM SAS treatment for 48 h could obtain the maximum inhibition rate (53.9%). In addition, SAS treatment caused a significant decrease in the mRNA and protein expression of xCT and GPX4, and a significant increase in ACSL4 expression in TE-1 cells treated with SAS. Flow cytometry results showed that the ferroptosis level was significantly increased after SAS treatment. However, the activation of ferroptosis by SAS was partially eliminated by treatment with ferrostatin-1 or Z-VAD (OH)-FMK. In conclusion, SAS inhibits the proliferation of esophageal carcinoma cells by activating the ferroptosis pathway.

Genome-wide screening for genomic aberrations in Kazakh patients with esophageal squamous cell cancer by comparative genomic hybridization.

Multiple chromosome aberrations are responsible for tumorigenesis of esophagus squamous cell carcinoma (ESCC). To characterize genetic alterations by comparative genomic hybridization (CGH) and their relation to ESCC, We enrolled 54 members with ESCC from Kazakh's patients. We found that the deletions of 3p (P = 0.032), 17p (P = 0.004), 22q (P = 0.000) and gains of 5p (P = 0.000), 11q (P = 0.000) were significantly correlated with the location of tumors. Losses of 1p (P = 0.005), 3p (P = 0.006), 22q (P = 0.024) and gains of 3q (P = 0.043), 8q (P = 0.038), 18q (P = 0.046) were also found more frequently in patients with larger diameter disease. The loss of 19q (P = 0.005) and gains of l3q (P = 0.045), 18p (P = 0.018) were significantly correlated with pathologic grade. The gain of 7p (P = 0.009) and deletion of 19q (P = 0.018) were seen more frequently in patients with Grade III-IV tumors. Chromosome amplifications in ESCC at 1q (P = 0.008), 7p (P = 0.008), 8q (P = 0.018) and deletions at 3p (P = 0.021), 11q (P = 0.002), 17p (P = 0.012) were related to lymph node metastasis; the gains of 1q (P = 0.026) and 6q (P = 0.017) and the loss of 11q (P = 0.001) were significant in different isoforms of HPV infection. We identified some chromosomes in which the genes were related to the tumorgenesis of ESCC, which may be a theme for future investigation.