Screening candidate microRNA-mRNA network for predicting the response to chemoresistance in osteosarcoma by bioinformatics analysis.

The search for biomarkers is important for providing more targeted treatments for osteosarcoma patients with chemoresistance. In this study, differentially expressed microRNAs (miRNAs) were identified from miRNA expression profiles. And the target messenger RNAs (mRNAs) of miRNA were obtained from two websites in public domains.

Salubrinal Enhances Doxorubicin Sensitivity in Human Cholangiocarcinoma Cells Through Promoting DNA Damage.

Cholangiocarcinoma (CCA) is a highly malignant and aggressive tumor of the bile duct that arises from epithelial cells. Chemotherapy is an important treatment strategy for CCA patients, but its efficacy remains limited due to drug resistance. Salubrinal, an inhibitor of eukaryotic translation initiation factor 2 alpha (eIF2α), has been reported to affect antitumor activities in cancer chemotherapy.

Reduction in activating transcription factor 4 promotes carbon tetrachloride and lipopolysaccharide/D‑galactosamine‑mediated liver injury in mice.

Although activating transcription factor 4 (ATF4) is involved in the regulation of numerous biological functions, whether ATF4 has a direct role in liver injury is unknown. The aim of the present study was to investigate the role of ATF4 in liver injury using mouse models. The results revealed that ATF4 protein is expressed markedly higher in the mouse liver when in comparison with other tissues.

Compound C induces protective autophagy in human cholangiocarcinoma cells via Akt/mTOR-independent pathway.

Compound C, a well-known inhibitor of AMP-activated protein kinase (AMPK), has been reported to exert antitumor activities in some types of cells. Whether compound C can exert antitumor effects in human cholangiocarcinoma (CCA) remains unknown. Here, we demonstrated that compound C is a potent inducer of cell death and autophagy in human CCA cells.

c‑Myc promotes cholangiocarcinoma cells to overcome contact inhibition via the mTOR pathway.

The loss of contact inhibition is a hallmark of a wide range of human cancer cells. Yet, the precise mechanism behind this process is not fully understood. c‑Myc plays a pivotal role in carcinogenesis, but its involvement in regulating contact inhibition has not been explored to date.