Vav1-dependent Rac1 activation mediates hypoxia-induced gemcitabine resistance in pancreatic ductal adenocarcinoma cells through upregulation of HIF-1α expression.

Hypoxia has been shown to induce gemcitabine (GEM) resistance in pancreatic ductal adenocarcinoma (PDAC) cells, however, the underlying mechanisms remain to be clarified. In the present study, we investigated whether activation of Vav1/Rac1/HIF-1α axis is responsible for hypoxia-induced GEM resistance in PDAC cells. Our results showed that Rac1 activation contributed to hypoxia-induced GEM resistance in PANC-1 cells.

Berberine Inhibits the Expression of SCT through miR-214-3p Stimulation in Breast Cancer Cells.

In this study, we aimed to evaluate the suppressive abilities of berberine (BBR) on MCF-7 and MDA-MB-231 cells and confirm its underlying mechanisms on miR-214-3p. We first built a panel of 18 miRNAs and 9 lncRNAs that were reported to participate in the mechanism of breast cancer. The RT-qPCR results suggested that BBR illustrated a dosage-dependent pattern in the stimulation to miR-214-3p in both MCF-7 and MDA-MB-231 cells.

Identification of key differentially expressed genes and gene mutations in breast ductal carcinoma in situ using RNA-seq analysis.

Background: The aim of this study was to identify the key differentially expressed genes (DEGs) and high-risk gene mutations in breast ductal carcinoma in situ (DCIS).

Methods: Raw data (GSE36863) were downloaded from the database of Gene Expression Omnibus (GEO), including three DCIS samples (DCIS cell lines MCF10.DCIS, Sum102, and Sum225) and one normal control sample (normal mammary epithelial cell line MCF10A).

DNA-PKcs is important for Akt activation and gemcitabine resistance in PANC-1 pancreatic cancer cells.

Pancreatic cancer is one of the most aggressive human malignancies with extremely poor prognosis. The moderate activity of the current standard gemcitabine and gemcitabine-based regimens was due to pre-existing or acquired chemo-resistance of pancreatic cancer cells. In this study, we explored the potential role of DNA-dependent protein kinase catalytic subunit (DNA-PKcs) in gemcitabine resistance, and studied the underlying mechanisms.

Overexpression of GOLPH3 is associated with poor clinical outcome in gastric cancer.

This study aims to investigate the expression and significance of GOLPH3 in human gastric cancer progression and prognosis. Using immunohistochemistry (IHC) and real-time reverse transcriptase polymerase chain reaction assay, we identified abnormally elevated expression of GOLPH3 in gastric cancer tissues compared to paired normal stomach mucosa tissues in 40 patients. In addition, the enzyme-linked immunosorbent assay (ELISA) was used to quantify serum GOLPH3 concentrations in the same 40 gastric cancer patients and 40 healthy individuals.