Fig. 4: NAT10 promoted the anti-apoptotic ability and Lenvatinib resistance of ERS hepatoma cells. | Cell Death Discovery

Fig. 4: NAT10 promoted the anti-apoptotic ability and Lenvatinib resistance of ERS hepatoma cells.

From: Role of NAT10-mediated ac4C-modified HSP90AA1 RNA acetylation in ER stress-mediated metastasis and lenvatinib resistance in hepatocellular carcinoma

Fig. 4

A–C The effects of siRNA-NAT10 and its inhibitor Remodelin (B, C) on the apoptosis of Huh-7 cells and Hep3B cells after NAT10 knockdown and inhibition were analyzed by flow cytometry (n = 3). D Western blot showed the expression levels of Bax, Bak apoptotic protein, and Bcl-2 anti-apoptotic protein genes in Huh-7 and hep3B cells after NAT10 knockdown or inhibition. The effect of siRNA-NAT10 (E) and its inhibitor Remodelin (F, G) on the sensitivity of Huh-7 cells and Hep3B cells to Lenvatinib after NAT10 knockdown and inhibition was analyzed by flow cytometry (n = 3). H CCK-8 assay was used to study the effects of NAT10 knockdown or inhibition on the viability of Huh-7 and Hep3B cells treated with different concentrations of Lenvatinib for 24 and 48 h. I Photographic images of xenograft tumors collected (n = 5). J Schematic diagram of mouse xenograft tumor administration. K Average tumor volume and weight of xenograft mice in the groups on day 21. L HE staining of mouse metastatic tumors. All groups of cells were subjected to TM induction 24 h in advance, and each experiment was conducted three times. Data were shown as mean ± standard deviation. *P < 0.05, **P < 0.01, ***P < 0.001.

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