LINC00261 inhibits progression of pancreatic cancer by down-regulating miR-23a-3p.

Long noncoding RNAs (lncRNAs) are usually dysregulated in the progression of pancreatic cancer. This research aims to explore the function and mechanism of LINC00261 in pancreatic cancer cell viability, invasion and apoptosis. Cancer Genome Atlas (TCGA) database was applied to analyze the association between survival probability of patients and level of LINC00261 or miR-23a-3p in pancreatic cancer. Quantitative reverse transcription polymerase chain reaction was conducted to analyze the levels of LINC00261 and miR-23a-3p. Cell viability, invasion and apoptosis of pancreatic cancer cells were determined via MTT, transwell invasion assay, and flow cytometry, respectively. The target relationship between LINC00261 and miR-23a-3p was determined via dual-luciferase reporter and RNA immunoprecipitation assays. Low level of LINC00261 indicated low survival probability of pancreatic cancer patients. LINC00261 level was decreased in pancreatic cancer cells than that in normal pancreatic ductal epithelial cells. Addition of LINC00261 restrained cell viability and invasion and facilitated apoptosis. miR-23a-3p was negatively correlated with LINC00261 level and high expression of miR-23a-3p indicated low survival probability. miR-23a-3p was targeted by LINC00261 and attenuated the influence of LINC00261 on pancreatic cancer cell viability, invasion and apoptosis. In conclusion, LINC00261 overexpression repressed cell viability and invasion and enhanced apoptosis by decreasing miR-23a-3p expression in pancreatic cancer cells, indicating a new target for the treatment of pancreatic cancer.

Scoulerine promotes cell viability reduction and apoptosis by activating ROS-dependent endoplasmic reticulum stress in colorectal cancer cells.

Scoulerine, an isoquinoline alkaloid isolated from Corydalis plants, has been reported to possess potent anti-proliferative and pro-apoptotic function in cancer cells. However, the effects and underlying mechanisms of scoulerine on colorectal cancer (CRC) progression remain elusive. CCK-8 and LDH assays were used to evaluate cell viability. Apoptosis was assessed by flow cytometry analysis, caspase-3/7 activity assay, and Western blot analysis of Bax, Bcl-2 and cytochrome c (Cyt C) expression. Oxidative stress level was examined by measuring reactive oxygen species (ROS) and glutathione (GSH) contents and superoxide dismutase (SOD) activity. Endoplasmic reticulum (ER) stress activation was detected by Western blot analysis of glucose-regulated protein 78 (GRP78) and C/EBP homologous protein (CHOP) expression. Results showed that scoulerine dose-dependently suppressed CRC cell viability. Scoulerine induced apoptosis and increased caspase-3/7 activity in CRC cells. Bax and cytosolic Cyt C expression was enhanced while Bcl-2 and mitochondrial Cyt C expression was reduced in scoulerine-treated CRC cells. Additionally, scoulerine induced oxidative damage in CRC cells by increasing ROS generation and reducing GSH content and SOD activity. Scoulerine activated ER stress, as evidenced by the increased GRP78 and CHOP expression in CRC cells. Interestingly, blocking ROS production by ROS scavenger N-acetyl-cysteine (NAC) attenuated scoulerine-induced ER stress. Inhibition of ER stress by 4-phenyl butyric acid (4-PBA) abolished scoulerine-induced ROS generation in CRC cells. Blockage of ROS and ER stress attenuated scoulerine-induced cell viability reduction and apoptosis in CRC cells. In conclusion, scoulerine promoted cell viability reduction and apoptosis by activating ROS-dependent ER stress in CRC cells.

Silencing Tspan1 inhibits migration and invasion, and induces the apoptosis of human pancreatic cancer cells.

Pancreatic cancer (PCC) is one of the most dangerous types of tumor as it is very difficult to treat and its 5­year survival rate is <6%. To date, there have been no effective therapeutic strategies to treat PCC, thus, novel effective therapeutic methods are required. Tetraspanin 1 (Tspan1) is a novel member of the tetraspanins superfamily and is highly expressed in a variety of types of cancer, including gastric, hepatocellular and colonic carcinomas. However, the detailed functional role of Tspan1 in pancreatic cancer cells is still unclear and further investigation is required to uncover its therapeutic potential for the treatment of different tumor types. The purpose of the present study was to investigate the expression of Tspan1 in human PCC tissues and cells, and explore the effect of Tspan1 silencing on invasion, migration, cell survival and apoptosis in human PCC to clarify its function. Expression levels of Tspan1 were analyzed in human pancreatic cancer tissues and the cell lines Capan­2 and SW1990 using immunohistochemistry staining, reverse transcription­quantitative polymerase chain reaction and western blotting. The effects of downregulation of Tspan1 expression on cell survival, apoptosis, invasion and migration were investigated viaTspan1­small interfering (si)RNA transfection into human PCC cell lines. The results indicated that Tspan1 expression was increased in human PCC tissues compared with the adjacent normal pancreatic tissues. Tspan1 was highly expressed in the human PCC cell lines Capan­2 and SW1990 when compared with the normal pancreatic cell line HPC­Y5. In addition, transfection with siRNA­targeting Tspan1 significantly reduced cell migration and invasion, and increased the cell apoptosis of Capan­2 and SW1990. The present findings highlighted the important role of Tspan1 in human PCC cell migration, invasion and apoptosis. Thus, Tspan1 RNA interference may serve as a potential therapeutic strategy to treat human PCC.