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. 2017 Feb 13;12(2):e0171827. doi: 10.1371/journal.pone.0171827

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© 2017 Arora et al

This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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Fig 4 — A Triptolide induced cell death in gastric cancer is mediated via Sp1. Treatment with 100nM triptolide decreased the mRNA expression of Sp1, HSF1 and HSP70 in MKN28 and MKN45 gastric adenocarcinoma cells in a time (24–48 hours) dependent manner. B. Protein expression of Sp1, HSP70 and HSF1 decreased after 100nM triptolide treatment in both MKN28 and MKN45 cells. C. Treatment of MKN28 and MKN45 cells with mithramycin (a chemical inhibitor of Sp1) led to a reduction in cell viability in a dose (25–200nM) as well as time (24–72 hours) dependent manner similar to triptolide. D. Treatment of MKN28 and MKN45 cells with 100nM mithramycin led to a time (24–48 hours) dependent decrease in the mRNA expression of HSF1 and HSP70, indicating that they lie downstream of Sp1. E. Treatment of MKN45 cells with 100nM mithramycin led to a time (24–48 hours) dependent decrease in the protein expression of HSF1 and HSP70, indicating that they lie downstream of Sp1 in gastric adenocarcinoma cells. F. Overexpression of Sp1 in gastric cancer cell line MKN28 and MKN45 resulted in a rescue from the triptolide induced cell death. * indicates p value < 0.05 when compared to untreated.