Novel STAT3 oligonucleotide compounds suppress tumor growth and overcome the acquired resistance to sorafenib in hepatocellular carcinoma.

Signal transducer and activator of transcription 3 (STAT3) plays an important role in the occurrence and progression of tumors, leading to resistance and poor prognosis. Activation of STAT3 signaling is frequently detected in hepatocellular carcinoma (HCC), but potent and less toxic STAT3 inhibitors have not been discovered. Here, based on antisense technology, we designed a series of stabilized modified antisense oligonucleotides targeting STAT3 mRNA (STAT3 ASOs).

Human augmenter of liver regeneration is important for hepatoma cell viability and resistance to radiation-induced oxidative stress.

To gain new insight into the biological function of the human augmenter of liver regeneration (hALR) in HCC, we studied its involvement in radiation-induced damage and recovery of HCC cells. We found that hALR expression was up-regulated in both HCC tissues and multiple hepatoma cell lines and correlated significantly with increased radiation clonogenic survival after radiation treatment. Exogenous expression of hALR increased radiation resistance in SMMC-7721 cells, and the increased survival was accompanied by a decrease in apoptosis and a prolonged G(2)-M arrest after irradiation.

[Efficient expression of exogenous human gp96 gene in tumor cells].

Background & Objective: Immunization of mice with preparations of heat shock protein(HSP) gp96 isolated from cancer cells has been shown to elicit specific protective cytotoxic T lymphocyte response against cells from which gp96 originate. This phenomenon exploits a new practicable pathway for cancer immunotherapy. But gp96 is generally expressed at low level in cells.