Hepatitis B virus X protein promotes CREB-mediated activation of miR-3188 and Notch signaling in hepatocellular carcinoma.

Familiar clustering of hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC) has been frequently reported. However, limited information is available about the underlying molecular mechanisms in HBV-related HCC patients with family history of HCC. In our previous study, Agilent miRNA Base 16.

Minocycline and cisplatin exert synergistic growth suppression on hepatocellular carcinoma by inducing S phase arrest and apoptosis.

Minocycline, a semisynthetic tetracycline, is a highly lipophilic molecule capable of infiltrating tissues and blood. Previous studies have revealed the functions and mechanisms of minocycline in anti-inflammation, protection of the nervous system and certain tumors. The role of minocycline has never been investigated in hepatocellular carcinoma (HCC).

Down-regulated KLF17 expression is associated with tumor invasion and poor prognosis in hepatocellular carcinoma.

Although the role of Krüppel-like factor 17 (KLF17) in regulating epithelial-mesenchymal transition (EMT) has been explored in breast cancer, its influence on primary hepatocellular carcinoma (HCC) remains unclear. This study aims to investigate the expression status of KLF17 in hepatocellular carcinoma (HCC) and the correlation between KLF17 expression and metastatic potential of HCC. KLF17 expression in HCC and adjacent liver tissues was studied by real-time PCR and Western blot, and the relationship between KLF17 expression and the clinicopathological features of HCC was evaluated in 60 patients.