Inhibitory effects of shRNA on expression of JNK1 and migration and invasion in mouse hepatocellular carcinoma cell lines mediated by ultrasound-targeted microbubble destruction

Zhang, Yuhong; Wu, Jun; Wang, Zihang; Dao-zi, Xia; Li, Guangsen; You, Yue; Huang, Dongmei; Bo, Huaying; Hu, Bin; Tang, Jianwu

doi:10.1016/j.biopha.2015.12.026

Cited by 2 publications

(1 citation statement)

References 33 publications

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“…In the early stages of HCC, HNF4A could inhibit cell proliferation of HCC through the miR-122-adam17 pathway ( Yang et al, 2020 ), and downregulation of HNF4A could lead to loss of hepatocyte characteristics ( Ramesh and Ganesan, 2016 ). The higher expression of MAPK8 is correlated to the lower tumor recurrence for HCC patients ( Gao et al, 2018 ), and upregulation of MAPK8 could inhibit the proliferation, migration, and invasion abilities of mouse HCC cell lines ( Zhang et al, 2016 ). NR3C1 encodes glucocorticoid receptors and is considered to be a tumor suppressor gene, which controls cell proliferation, differentiation, and apoptosis ( Matthews et al, 2015 ).…”

Section: Discussionmentioning

confidence: 99%

Network pharmacology and in vitro experiments-based strategy to investigate the mechanisms of KangXianYiAi formula for hepatitis B virus-related hepatocellular carcinoma

Cao

Chen

et al. 2022

Front. Pharmacol.

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The Chinese traditional medicine KangXianYiAi formula (KXYA) is used to treat hepatic disease in the clinic. Here we aim to confirm the therapeutic effects and explore the pharmacological mechanisms of KXYA on hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC). We first collected and analyzed clinical data of 40 chronic hepatitis B (CHB) patients with precancerous liver lesions under KXYA treatment. Then, the cell viability, migration, cell cycle, and apoptosis of HepAD38 cells with KXYA treatment were examined. Next, we performed network pharmacological analysis based on database mining to obtain the key target pathways and genes of KXYA treatment on HBV-related HCC. We finally analyzed the expression of the key genes between normal and HBV-related HCC tissues in databases and measured the mRNA expression of the key genes in HepAD38 cells after KXYA treatment. The KXYA treatment could reduce the liver nodule size of CHB patients, suppress the proliferation and migration capabilities, and promote apoptosis of HepAD38 cells. The key pathways of KXYA on HBV-related HCC were Cancer, Hepatitis B, Viral carcinogenesis, Focal adhesion, and PI3K-Akt signaling, and KXYA treatment could regulate the expression of the key genes including HNF4A, MAPK8, NR3C1, PTEN, EGFR, and HDAC1. The KXYA exhibited a curative effect via inhibiting proliferation, migration, and promoting apoptosis of HBV-related HCC and the pharmacological mechanism was related to the regulation of the expression of HNF4A, MAPK8, NR3C1, PTEN, EGFR, and HDAC1.

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