Truepotter3531
Knockdown of SNHG17 caused the inhibition on CRA cell proliferation and migration. SNHG17 promoted CRA cell proliferation and migration by sponging miR-23a-3p to upregulate CXCL12.
SNHG17 promotes the proliferation and migration of CRA cells by inhibiting miR-23a-3p to modulate CXCL12-mediated angiogenesis.
SNHG17 promotes the proliferation and migration of CRA cells by inhibiting miR-23a-3p to modulate CXCL12-mediated angiogenesis.
Protein regulator of cytokinesis 1 (PRC1) has been reported to play important role in the pathogenesis of various cancers. However, its role in colon cancer has not been studied. Here, we aimed to investigate the biological functions and potential mechanism of PRC1 in colon cancer.
The expression level of PRC1 in colon cancer tissues and cell lines was detected by quantitative real-time polymerase chain reaction (qRT-PCR), Western blotting, and immunohistochemical (IHC) staining of a tissue microarray (TMA). Furthermore, colon cancer cell lines HCT116 and SW480 were treated with short hairpin RNAs against PRC1. The biological function of PRC1 was determined by MTT proliferation, colony formation assay, cell cycle, and apoptosis assays. Then, an in vivo tumor formation assay was conducted to explore the effects of PRC1 on tumor growth.
The mRNA and protein expression levels of PRC1 were highly expressed in colon cancer tissues and cell lines. WAY-309236-A ic50 PRC1 expression was associated with clinicopathological charac These findings showed the potential of PRC1 to be used for therapeutic approaches in colon cancer.
There is evidence that circSMYD4 is differentially expressed in hepatocellular carcinoma (HCC), but its mechanism of action remains unclear. Therefore, this study aimed to explore the role of circSMYD4 in the occurrence and development of HCC and its specific molecular mechanism.
The expressions of related genes and proteins in the development of HCC were detected by real-time quantitative-PCR and Western blot. HCC cells treated with RNase R and Actinomycin D were used to examine the stability of circSMYD4. Bioinformatics analysis, RNA pull-down assay, luciferase assay and Spearman correlation analysis were performed to evaluate the interaction between circSMYD4 and miRNA. Cell Counting Kit-8, clone formation assay, wound healing assay, Transwell, flow cytometry, nude tumor formation experiment, and immunohistochemistry were employed to analyze the function of circSMYD4 in HCC. A rescue experiment was conducted to analyze the effect of miR-584-5p on the physiological functions of cells.
CircSMYD4 was down-regulated in HCC tissues and cells, and was not easily affected by RNase R and Actinomycin D. The abundances of circSMYD4 and SMYD4 in the cytoplasm were significantly higher than in the nucleus. Up-regulation of circSMYD4 inhibited the proliferation, invasion and migration and promoted the apoptosis of HCC cells in vitro, while it inhibited tumor growth, promoted apoptosis-related proteins, and suppressed alpha-fetoprotein (AFP) levels in vivo. CircSMYD4 could be used as a miRNA sponge to target miR-584-5p. In addition, miR-584-5p overexpression partially reversed the regulatory effect of circSMYD4 on HCC.
CircSMYD4 prevents the development of HCC through regulating multiple signaling pathways such as metastasis and apoptosis by sponging miR-584-5p.
CircSMYD4 prevents the development of HCC through regulating multiple signaling pathways such as metastasis and apoptosis by sponging miR-584-5p.Physical activity at workplace can positively impact various wellbeing outcomes yet developing and implementing exercise programs that are straightforward, time-efficient and widely applicable remains a notable public health challenge. Sport4Health Network (SPORT4H) project co-funded by the European Union Erasmus+ programme unites health and sport professionals in an effort to encourage participation in physical activity among working population and reduce health risk factors for lifestyle diseases. A two-day SPORT4H scientific forum on non-traditional types of work-place exercise interventions was organized from 14th to 15th September 2020, to critically evaluate evidence on stretching and resistance exercise programs targeted to working population in aim to identify knowledge gaps and future areas of research and application. Evidence on traditional interventions (e.g., walking initiatives, active travel) appears more robust while only few studies evaluated the applicability of non-traditional PA programs in working population. However, we identified a moderate-to-strong link between non-traditional PA programs at the workplace and several health-related physical fitness indices, with resistance exercise turned out to be superior to other exercise interventions analyzed. It appears that low-volume high-repetition resistance exercise favorably affects musculoskeletal disorders, work performance and health-related quality of life in employees who exercised at least 3 times per week for over 8 weeks. In terms of safety, screening protocols should employ health-related questionnaires, adopting a progressive training load, and prescribing training programs to individual participants' needs. Implementing non-traditional PA programs aimed to improve health-related physical fitness and counteract sedentary behavior at workplace might be therefore of utmost importance to contribute to health promotion in this sensible population.
RAS association domain family protein 1A (RASSF1A) promoter hypermethylation is suggested to be linked to hepatocellular carcinoma (HCC), but the results remained controversial.
We evaluated how RASSF1A promoter hypermethylation affects HCC risk and its clinicopathological characteristics through meta-analysis. Data on DNA methylation in HCC and relevant clinical data were also collected based on The Cancer Genome Atlas (TCGA) database to investigate the prognostic role of RASSF1A promoter hypermethylation in HCC.
Forty-four articles involving 4777 individuals were enrolled in the pooled analyses. The RASSF1A promoter methylation rate was notably higher in the HCC cases than the non-tumor cases and healthy individuals, and was significantly related to hepatitis B virus (HBV) infection-positivity and large tumor size. Kaplan-Meier survival analysis revealed that HCC cases with RASSF1A promoter hypermethylation had worse outcomes. Receiver operating characteristic curves confirmed that RASSF1A promoter methylation may be a marker of HCC-related prognoses.
