ABSTRACT
Abstract Objectives Emerging evidence has demonstrated that LINC01857 exerts a pivotal function in many cancers. However, its function in Pancreatic Ductal Adenocarcinoma (PDAC) still remains unclear. This study was designed to investigate the regulatory character of LINC01857 in PDAC. Methods Bioinformatic tools and databases were used to seek potential miRNAs and mRNAs. Gene expression was evaluated by Reverse Transcription quantitative real-time Polymerase Chain Reaction (RT-qPCR), and western blot was used for protein level detection. A subcellular fraction assay was done to ascertain the location of LINC01857 in PANC-1 and BxPC-3 human pancreatic cancer cells. CCK-8, EdU, wound healing and Transwell assays were performed to inquire into the influence of LINC01857, and SPARC -related Modular Calcium-binding protein-2 (SMOC2) on cell viability, proliferation, migration, and invasion, respectively. The interaction between LINC01857 and its downstream genes was explored by RNA immunoprecipitation and luciferase reporter assays. Results LINC01857 levels were significantly elevated in PDAC. Knockdown of LINC01857 significantly restrained the proliferation, migration, invasion, and Epithelial-Mesenchymal Transition (EMT) process of PDAC cells. MiR-19a-3p was a downstream target of LINC01857, and miR-19a-3p levels were significantly decreased in PDAC cells. In addition, SMOC2 expression had a negative correlation with that of miR-19a-3p, and SMOC2 was a downstream target of miR-19a-3p. Furthermore, SMOC2 upregulation partially abolished the inhibitive influence of LINC01857 downregulation on cell proliferation, migration, invasion, and the EMT process. Conclusion LINC01857 promotes malignant phenotypes of PDAC cells via upregulation of SMOC2 by interacting with miR-19a-3p. HIGHLIGHTS LINC01857 is upregulated in PAAD and promotes malignant cellular behaviors. LINC01857 interacts with miR-19a-3p to regulate SMOC2 expression. LINC01857 promotes malignant cellular phenotypes by upregulating SMOC2.
ABSTRACT
Mental fatigue, first known as brain fag, is one of the common clinical fatigue types. Due to the increase of the intensity and proportion of mental work, mental fatigue has an increasing prevalence among the people working in all fields especially, especially in the military field. In recent years, mental fatigue has become an important part of fatiguerelative research. How to prevent, control and alleviate mental fatigue is an important issue, which is based on evaluating or determining the degree of mental fatigue. Because mental fatigue has strong subjectivity and its mechanism is still unclear, there are many evaluation methods, but with no unified standard. This article reviews the evaluation methods of mental fatigue, including symptomatic, psychobehavioral, and physiological and biochemical assessment, and discusses the main contents and principles of various evaluation methods, so as to provide reference to mental fatigue research.
ABSTRACT
Objective @# To investigate the effect of mitochondrial fission protein 1 (FIS1) on apoptosis and cisplatin resistance in tongue squamous cell carcinoma (TSCC) cells.@*Methods @#The squamous cell carcinoma cell lines SCC9 and CAL27 were used to detect the mRNA and protein levels of FIS1 after cisplatin treatment, the knockdown and overexpression of FIS1 of SCC9 and CAL27 with or without cisplatin treatment were accomplished through small interfering RNA (siRNA) and plasmid, respectively. The mitochondrial division state in cells was detected by mitochondrial staining, and the apoptosis state of cells was detected by TUNEL, flow cytometry and Caspase 3/7.@*Results@#FIS1 protein expression in tongue squamous carcinoma cells treated with cisplatin was increased, but the mRNA level did not change. Silencing of FIS1 expression reduced mitochondrial division and apoptosis in squamous cell carcinoma cells treated with cisplatin, whereas overexpression of FIS1 exhibited the opposite effects. The percentage of dividing mitochondria, the number of apoptotic cells and the activity of Caspase 3/7 in SCC9 and CAL27 cells were significantly different before and after modulation of FIS1 expression (P < 0.05). @*Conclusion@#FIS1 is involved in the regulation of cisplatin chemotherapy sensitivity in tongue squamous cell carcinoma and can be used as a new target for improving the sensitivity of cisplatin chemotherapy in oral squamous cell carcinoma.