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. 2020 Aug 10;9(19):6972–6983. doi: 10.1002/cam4.3331

Figure 3.

Figure 3

PI16 knockdown improves sorafenib response in HCC via activating p38 MAPK/caspase‐dependent apoptosis. (A) Representative markers of apoptosis, PI3K/AKT and MAPK signaling in PI16 knockdown MHCC‐97H cells treated by 5 μM Sorafenib determined by Western blot; Total AKT, total p‐p38 MAPK, and β‐actin were used as controls. (B and C) Representative flow cytometry images of Annexin V‐PI staining and quantification of net apoptosis in PI16 knockdown MHCC‐97H cells treated with 5 μM Sorafenib, and in the absence or presence of SB203580. (D) Cell cytotoxicity LDH assay of PI16 knockdown MHCC‐97H cells treated with 5 μM Sorafenib, and in the absence or presence of SB203580. (E) Protein levels of cleaved caspase 3 and cleaved PARP determined by Western blot in PI16 knockdown MHCC‐97H cells treated with 5 μM Sorafenib, and in the absence or presence of SB203580; β‐actin was used as a control. ***P < .001, Student's t test