KMT2D deficiency enhances the anti-cancer activity of L48H37 in pancreatic ductal adenocarcinoma

doi:10.4251/wjgo.v11.i8.599

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World Journal of Gastrointestinal Oncology

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1948-5204

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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA

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World J Gastrointest Oncol. Aug 15, 2019; 11(8): 599-621
Published online Aug 15, 2019. doi: 10.4251/wjgo.v11.i8.599

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Figure 5 KMT2D knockdown augments L48H37-induced apoptosis and blocks migration in vitro. A, B: Venn diagram showing overlapping DEGs in KMT2D knockdown Colo357 and SUIT-2 cells. Upregulated genes are shown in blue and red, and the downregulated in yellow and green in the Colo357 and SUIT-2 cells, respectively; C, D: Functional analysis of the overlapping DEGs; E, F: Graph showing the number of manually tracked migrating control and KMT2D knockdown SW1990 cells treated with L48H37.

Citation: Li SS, Jiang WL, Xiao WQ, Li K, Zhang YF, Guo XY, Dai YQ, Zhao QY, Jiang MJ, Lu ZJ, Wan R. KMT2D deficiency enhances the anti-cancer activity of L48H37 in pancreatic ductal adenocarcinoma. World J Gastrointest Oncol 2019; 11(8): 599-621
URL: https://www.wjgnet.com/1948-5204/full/v11/i8/599.htm
DOI: https://dx.doi.org/10.4251/wjgo.v11.i8.599