ABSTRACT
[This corrects the article DOI: 10.1155/2020/6206157.].
ABSTRACT
BACKGROUND: The cell cycle pathway genes are comprised of 113 members which are critical to the maintenance of cell cycle and survival of tumor cells. This study was performed to investigate the diagnostic and prognostic values of cell cycle gene expression in hepatocellular carcinoma (HCC) patients. METHODS: Clinical features and cell cycle pathway gene expression data were obtained from the Gene Expression Omnibus and The Cancer Genome Atlas databases. Differentially expressed genes (DEGs) were determined by the student t-test between HCC and noncancerous samples. Kaplan-Meier survival, univariate, and multivariate survival analyses and validation analysis were performed to characterize the associations between cell cycle gene expression and patients' overall survival and recurrence-free survival. RESULTS: 47 and 5 genes were significantly upregulated and downregulated genes in HCC samples, respectively. The high expression of BUB3, CDK1, and CHEK1 was associated with increased mortality (adjusted P value = 0.04, odds ratio (OR): 1.89 (95% confidence interval (CI): 1.04-3.46); adjusted P value = 0.02, OR: 2.06 (95% CI:1.15-3.75); and adjusted P value = 0.04, OR: 1.84 (%95 CI: 1.03-3.32), respectively). The expression of PTTG2 and RAD21 was significantly associated with cancer recurrence (adjusted P value = 0.01, OR: 2.17 (95% CI: 1.24-3.86); adjusted P value = 0.03, OR: 1.88[95% CI:1.08-3.28], respectively), while the low expression of MAD1L1 was associated with cancer recurrence (adjusted P value = 0.03, OR: 0.53 (%95 CI: 0.3-0.93)). CONCLUSIONS: The present study demonstrated that BUB3, CDK1, and CHEK1 may serve as a prognostic biomarker for HCC patients. PTTG2, RAD21, and MAD1L1 expression is a major factor affecting the recurrence of HCC patients.
Subject(s)
Biomarkers, Tumor/genetics , Carcinoma, Hepatocellular/diagnosis , Carcinoma, Hepatocellular/genetics , Genes, cdc , Liver Neoplasms/diagnosis , Liver Neoplasms/genetics , Adult , Computational Biology , Female , Humans , Male , Middle Aged , Prognosis , Sensitivity and Specificity , Survival AnalysisABSTRACT
BACKGROUND: Accumulated evidences have demonstrated that long non-coding RNAs (lncRNAs) are dysregulated and correlate with the pathophysiological basis of malignant tumors. The objective of this research is to uncover the possible molecular mechanism of MACC1-AS1 regarding the regulation of pancreatic carcinoma (PC) metastasis. METHODS: lncRNA microarray and qRT-PCR were applied to identify differentially expressed lncRNA profile in PC. The function and role of MACC1-AS1 in PC were assessed via in vitro as well as in vivo assays. Luciferase analyses, RNA immunoprecipitation, and RNA pull-down were performed to determined the underlying MACC1-AS1 mechanisms. RESULTS: Numbers of differentially expressed lncRNAs in PC were identified via lncRNA microarrays, among which MACC1-AS1 was revealed as the most abundant lncRNA. The upregulation of MACC1-AS1 in PC was further confirmed in two expanded PC cohorts, which showed that MACC1-AS1 expression was upregulated in those PC patients with poor survival. Functionally, knockdown of MACC1-AS1 inhibited the proliferation as well as metastasis of PC cells. Meanwhile, MACC1-AS1 upregulated the expression of PAX8 protein, which promoted aerobic glycolysis and activated NOTCH1 signaling. Additionally, PAX8 was upregulated in PC tissues, which was correlated with the expression of MACC1-AS1 and the overall survival of PC patients. CONCLUSIONS: Together, our findings indicate a critical role of MACC1-AS1/PAX8/NOTCH1 signaling, which may be an alternative treatment target in PC therapy.
Subject(s)
PAX8 Transcription Factor/metabolism , Pancreatic Neoplasms/genetics , Pancreatic Neoplasms/metabolism , RNA, Long Noncoding/genetics , Receptor, Notch1/metabolism , Signal Transduction , Trans-Activators/genetics , Adult , Aged , Animals , Apoptosis/genetics , Biomarkers, Tumor , Cell Cycle , Cell Line, Tumor , Cell Proliferation , Disease Models, Animal , Disease Progression , Female , Gene Expression Profiling , Gene Expression Regulation, Neoplastic , Humans , Immunohistochemistry , Male , Mice , Middle Aged , Models, Biological , Pancreatic Neoplasms/mortality , Pancreatic Neoplasms/pathology , Prognosis , Xenograft Model Antitumor Assays , Pancreatic NeoplasmsABSTRACT
OBJECTIVES: This study sought to determine ethnic difference in physical violence and to see if ethnicity is an independent predictor of violence by surveying eight Korean or Han ethnic elementary schools in Yanji city, China. A total of 2,316 school children from fourth through sixth grade participated the study. METHODS: Participants completed a questionnaire on sociodemographic background and experiences of physical violence during the previous year using the Conflict Tactics Scale. The history of physical violence was categorized as within the family, by peers, or by teachers. RESULTS: Han children reported significantly higher rates of physical abuse compared with Koreans (76.2% vs. 54.9%, chi2=116.12, df=1, p=<.001). Binary logistic regression analysis identified five risk factors for physical violence:(1) ethnic Han (odds ratio [OR]=3.01, 95% confidence interval [CI]=2.47-3.66), (2) boys (OR=2.76, 95% CI=2.28-3.36), (3) poor economic status (OR=1.69, 95% CI=1.17-2.42), (4) single or absent parents (OR=1.42, 95% CI=1.09-1.86), (5) interaction of fourth-graders with promotive or neutral opinions of corporal punishment (OR=2.41, 95% CI=1.86-3.13). Ethnicity remained an independent risk factor after other sociodemographic variables were controlled. CONCLUSION: These findings showed cross-cultural risk factors of child physical abuse, including ethnicity which previously identified as a factor in literature. This study particularly reports lower prevalence of physical violence in ethnic minority, Korean-Chinese, compared with the Han ethnic group. This result explained a special environment of Korean self-government district and the successful adaptation of the ethnic minority to the mainstream culture.