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CDK4 was identified as a potential target for miR-486-5p. LncRNA LINC01194 was able to inhibit miR-486-5p expression and upregulate the expression level of CDK4. Finally, the results of in vivo animal models confirmed that lncRNA LINC01194 promoted NSCLC progression by modulating the miR-486-5p/CDK4 axis. Conclusion LncRNA LINC01194 promoted the progression of NSCLC by modulating the miR-486-5p/CDK4 axis. © 2020 Xing et al.Background In a data mining search for potential therapeutic targets to improve the outcome of rectal cancer, we identified PCSK1 as the cell-cell signaling gene most significantly associated with poor response to concurrent chemoradiotherapy (CCRT). This study aims to investigate the prognostic value of PCSK1 expression in rectal cancer patients who underwent neoadjuvant CCRT. Methods Endoscopic biopsy specimens from 172 rectal cancer patients receiving neoadjuvant CCRT followed by curative surgery were assessed immunohistochemically for PCSK1 expression, and H-scores were determined. Expression levels of PCSK1 were further analyzed for correlations with clinicopathologic features, tumor regression grade, metastasis-free survival, disease-specific survival, and recurrence-free survival. Results PCKS1 overexpression was significantly associated with pretreatment tumor status (T3-4; p = 0.009), pretreatment nodal status (N1-2; p less then 0.001), posttreatment tumor status (T3-4; p less then 0.001), posttreatment nodal status (N1-2; p less then 0.001), vascular invasion (p = 0.003), and perineurial invasion (p = 0.023). PCKS1 overexpression was also found to be significantly associated with a lower degree of tumor regression (p less then 0.001). In the&nbsp;univariate analysis, PCSK1 overexpression was significantly associated with lower disease-specific survival, metastasis-free survival, and recurrence-free survival (p less then 0.005). PCSK1 overexpression remained an independent prognostic&nbsp;factor of lower disease-specific survival (p = 0.003; hazard ratio, 5.478) in the&nbsp;multivariate analysis. Conclusion Determination of PCSK1 overexpression may be useful for identifying rectal cancer patients at risk for a poor response and worse survival after CCRT. © 2020 Chou et al.Purpose This study aims to investigate the biological effect and molecular mechanism of Lamin B1(LMNB1) in lung cancer cells and its significance for the prognosis of lung adenocarcinoma(LUAD) patients. Methods In this study, Bioinformatics was performed to analyze the expression at mRNA level and prognosis effect of LMNB1 in LUAD from TCGA dataset. The immunohistochemistry(IHC) assay was conducted to analyzed the expression of LMNB1 at the protein level in LUAD tissues. The correlation between the expression of LMNB1 and the clinical factors in patients with LUAD was analyzed. [https://www.selleckchem.com/products/gdc6036.html learn more] Next, LMNB1 transfected into LUAD cell lines (A549 and PC-9) which was proved by Western blot. CCK8 assay, cloning formation assay, and xenograft assay were conducted to explore the effect and mechanism of LMNB1 on the proliferation of LUAD cell lines in vitro and in vivo. Results The results of the present study demonstrated that LMNB1 was highly expressed in LUAD tissues and related to tumor stage. High LMNB1 expression was related with more advanced clinicopathological factors such as low degree of differentiation (P=0.02), large tumor size (P less then 0.01), lymph node metastasis (P less then 0.01) and higher tumor stage (P less then 0.01). After knocking down LMNB1, the cell growth rate (P less then 0.01) and the number of colonies (P less then 0.01) were significantly reduced, and the level of the proliferating marker Ki67 (P less then 0.01) was significantly decreased. At the same time, in vivo experiments showed that the tumor volume and tumor of the mice were significantly reduced (P less then 0.01). Moreover, we found that knockdown LMNB1 can inhibit the proliferation of lung cancer cells by inhibiting AKT phosphorylation by Western blot. Conclusion In summary, LMNB1 play an of vital roles in the growth of LUAD cells, highlighting its potential as a therapeutic target for the treatment of LUAD patients. © 2020 Li et al.Background Increasing evidence has demonstrated the importance of non-coding RNAs including long non-coding RNA (lncRNA) and microRNAs (miRNAs) in the tumorigenesis of osteosarcoma (OS). Abnormal expression of lncRNA olfactory receptor family 3 subfamily A member 4 (OR3A4) was found in multiple human cancers; however, the function of OR3A4 in OS remains largely unknown. Materials and Methods The expression level of OR3A4 in OS tissues and cell lines was detected by RT-qPCR. Cell counting kit-8 assay, colony formation and flow cytometry analysis were performed to determine the growth of OS cells. The targets of OR3A4 were predicted using the miRDB database. The binding between OR3A4 and miRNAs was confirmed by dual-luciferase reporter assay. Results OR3A4 was overexpressed in OS tissues and correlated with the advanced progression of OS patients. Down-regulation of OR3A4 significantly inhibited the proliferation and colony formation of OS cells. Mechanistically, OR3A4 acted as a sponge of miR-1207-5p. Glucose-6-phosphate dehydrogenase (G6PD) was identified as a target of miR-1207-5p. Knockdown of OR3A4 increased the expression of miR-1207-5p and consequently, suppressed the level of G6PD in OS cells. Due to the essential role of G6PD in the pentose phosphate pathway (PPP), depletion of OR3A4 inhibited NADPH production, glucose consumption and lactate generation. Decreased level of NADPH by depletion of OR3A4 up-regulated the redox state (ROS) content and resulted in endoplasmic reticulum (ER) stress in OS cells. Restoration of G6PD significantly attenuated the cell growth inhibition induced by OR3A4 knockdown. Conclusion Our finding suggested the critical role of OR3A4 in the proliferation of OS cells via targeting the miR-1207-5p/G6PD axis. © 2020 Wang et al.Purpose A consensus about the pathogenesis of torus palatinus (TP) in patients receiving dialysis still eludes the scientific community. This prospective observational study investigated the epidemiology of TP in peritoneal dialysis and hemodialysis patients and analyzed the influences of multiple pathogenic factors such as mineral and bone disorders, genetic, environmental or nutritional triggers, progression of age, heredity, climatologic or biomechanical causes, and hyperparathyroidism on the formation of TP. Methods Between 2013 and 2016, a total of 575 chronic dialysis patients (441 on hemodialysis and 134 on peritoneal dialysis) were recruited from Chang Gung Memorial Hospital, Taiwan. Patients were stratified into two groups based on the presence (n = 179) or absence (n = 396) of TP. Demographic, oral examination, laboratory, and dialysis data were collected for analysis. Student's t-test was used to analyze the quantitative variables and Chi-square or Fisher's exact test for categorical variables. Univariate binary logistic regression analysis was conducted to determine the predictors for TP and multivariate binary logistic regression analysis to identify significant associated factors.