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. 2019 Jun 29;11(7):918. doi: 10.3390/cancers11070918

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© 2019 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Knockdown of eIF2α by gene silencing inhibits the extraordinary apoptosis effect in HCC. (A,B) siRNA knockdown of eIF2 expression downregulated p-eIF2α expression, and levels of cleaved caspase 3 or cleaved PARP also decreased, which promoted cell survival. Quantification of western blot using ImageJ, normalized to GAPDH. * p < 0.05, ** p < 0.01, *** p < 0.001 compared with the control group. (C) After the regulated expression of PP1 or eIF2α and treatment with or without fisetin to check cell apoptosis in liver cancer cells by flow cytometry. (D) Quantification of Figure 6C. Data indicate the percentage of apoptotic cells (annexin-V positive + annexin-V and propidium iodide (PI) double positive cells) (*p < 0.05, ** p < 0.01, *** p < 0.001) compared with the nontreatment group.

Knockdown of eIF2α by gene silencing inhibits the extraordinary apoptosis effect in HCC. (A,B) siRNA knockdown of eIF2 expression downregulated p-eIF2α expression, and levels of cleaved caspase 3 or cleaved PARP also decreased, which promoted cell survival. Quantification of western blot using ImageJ, normalized to GAPDH. * p < 0.05, ** p < 0.01, *** p < 0.001 compared with the control group. (C) After the regulated expression of PP1 or eIF2α and treatment with or without fisetin to check cell apoptosis in liver cancer cells by flow cytometry. (D) Quantification of Figure 6C. Data indicate the percentage of apoptotic cells (annexin-V positive + annexin-V and propidium iodide (PI) double positive cells) (*p < 0.05, ** p < 0.01, *** p < 0.001) compared with the nontreatment group.