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Investigation the mechanism of the apoptosis induced by lactacystin in gastric cancer cells

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Tumor Biology

Abstract

The study aims to investigate the relationship between nuclear factor (nuclear factor kappa B (NF-κB)) viability and lactacystin-mediated cell apoptosis in gastric cancer cells. Two gastric cancer cell lines (MKN28 and SGC7901) were treated with lactacystin—a proteasome inhibitor for 24 h. The cell viability, toxicity, and death were measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) method. DNA binding viability of NF-κB and caspase-3 viability were analyzed by ELISA; the expression of p65 NF-κB nuclear protein was detected by immunocytochemistry and Western blot. Lactacystin reduced DNA binding viability of NF-κB (t = 3.0,P = 0.013) and the NF-κB viability (compared to the 5, 10 μmol/L MKN28 cell (p53 mutant) line, P < 0.001) and the expression of p65 NF-κB nuclear protein decreased parallelled to concentrations of lactacystin in MKN28 cell line, while without obvious effects on NF-κB viability in SGC7901 cell line (P = 0.381), while the viability of caspase-3 increased also along with the raising of lactacystin concentrations (compared to control, 5 μmol/L: SGC7901 cell line P = 0.029, MKN28 cell line P < 0.001; 10 μmol/L: SGC7901 cell line, P < 0.001, MKN28 cell line, P < 0.001). It was concluded that lactacystin had diversified killing effects on gastric cancer cells. The mechanism may be related to induce the apoptosis by downregulation of nuclear factor kappa B viability. There may be additional cell survival/death pathway in SGC7901 gastric cancer cells.

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Correspondence to Yinghua Li.

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Li, Y., Gao, H., Wang, Y. et al. Investigation the mechanism of the apoptosis induced by lactacystin in gastric cancer cells. Tumor Biol. 36, 3465–3470 (2015). https://doi.org/10.1007/s13277-014-2982-x

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  • DOI: https://doi.org/10.1007/s13277-014-2982-x

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