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Objective: To investigate the prognostic factors of cutaneous malignant melanoma (CMM) and establish an effective nomogram survival prediction model. Materials and methods: The clinical data of patients diagnosed with stage M0 CMM from 2000 to 2019 in the Surveillance, Epidemiology, and End Results (SEER) database were collected and retrospectively analyzed. The variables that may be related to prognosis were analyzed by Lasso-Cox regression analysis using R software. Independent prognostic factors were screened. A nomogram model for predicting the prognosis of CMMC was drawn, and its accuracy was verified by c-index, NR, IDI and calibration curve. Results: A total of 2,679 patients with CMM were included. Lasso-Cox analysis showed that male sex, multiple tumors, higher T stage, SEER stage, widowed, divorced, and separated often indicated poor prognosis. The nomogram model calibration curve was in good agreement with the ideal curve, and the C-index was 0.734 in the training group and 0.761 in the validation group, respectively. In the training group, the AUC of 1-, 3-, 5- and 8-year survival were 0.80, 0.75, 0.74 and 0.72, respectively. In the validation group, the AUC of 1-, 3-, 5- and 8-year survival were 0.75, 0.79, 0.78 and 0.79, respectively. NRI and IDI were superior to the prediction ability of TNM stage and SEER stage (p < 0.05). The established prognostic score can divide patients into high and low score groups with significant prognostic difference (p < 0.05). Conclusions: Sex, SEER stage, T stage, total number of tumors and marital status are independent prognostic factors for CMM patients, and the nomogram model presented a better performance than TNM stage and SEER stage in predicting the prognosis of CMM patients. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To explore the correlation between gene polymorphism and opioid efficacy in patients with gastric or intestinal cancer. PATIENTS AND METHODS: Fifty-nine patients who underwent laparoscopic surgery for gastric or intestinal cancer under general anesthesia were included and randomly divided into oxycodone (n=30) and sufentanil groups (n=29) by reproducible random number generation method. Single nucleotide polymorphisms (SNPs) of four alleles: μ-opioid receptor gene OPRM1 A118G, cytochrome P450 (CPY450) enzyme system: CPY3A4*1G, CYP3A5*3, and CYP2D6*10 were detected by PCR-pyrosequencing. Patients in sufentanil group received intravenous sufentanil injection during anesthesia induction, intraoperative maintenance, and postoperative analgesia, while those in oxycodone group received oxycodone. Patients’ postoperative VAS score, opioid use, and prevalence of adverse reactions were recorded. RESULTS: The genotype distribution of OPRM1 A118G, CYP3A4*1G, CYP3A5*3, and CYP2D6*10 in Chinese gastric cancer/intestinal cancer patients accorded with the Hardy-Weinberg law (p>0.05). OPRM1 A118G polymorphism correlated with postoperative VAS score and medication dosage, in oxycodone group (p<0.05), while it didn’t with those of sufentanil group. The VAS scores in GG group were higher than that in AA group and AG group at T6-T9, (p<0.05); the postoperative pain remedies times in GG group were more than that in the AA and AG groups (p=0.002). CYP3A4*1G polymorphism related to postoperative VAS score, medication dosage and prevalence of adverse reactions in sufentanil group (p<0.05), while it didn’t with those of oxycodone group (p>0.05). The total intraoperative medication in AA group was less than that in GG and GA groups (p<0.01), with a higher prevalence of respiratory depression (p=0.01). Nor was there any correlation of CYP3A5*3 and CYP2D6*10 polymorphisms with the efficacy, postoperative VAS score, pain remedies times, postoperative 24 h medication dosage, or prevalence of adverse reactions in oxycodone and sufentanil groups. CONCLUSIONS: Gene polymorphism affects the efficacy and adverse reactions of opioids in patients undergoing laparoscopic gastric or intestinal cancer surgery. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To explore whether ischemic postconditioning will lighten hepatic apoptosis caused by hepatic ischemia/reperfusion injury by inhibiting the mitochondria pathway. MATERIALS AND METHODS: Pathomorphology of hepatic tissues in rats was observed under an optical microscope after hematoxylin-eosin (HE) staining. Hepatic apoptosis was detected using agarose gel electrophoresis (AGE) with DNA fragments and flow cytometry. Changes in morphology structure of mitochondria in hepatocytes of rats were observed under an electron microscope. Changes in mitochondria transmembrane potential of hepatocytes of rats were detected using a laser scanning confocal microscope (LSCM). Western blotting was adopted to detect changes in the expression of caspase-3 and cytochrome C protein in hepatocytes of rats. RESULTS: Compared with that in I/R group, swelling degree of mitochondria in most hepatocytes of rats in ischemic postconditioning (IPOST) group and IPC group was lighter. Changes in expression of caspase-3 and cytochrome C protein in hepatic cells of rats: caspase-3 was lowly expressed and cytochrome C was highly expressed in S group. The expression of caspase-3 was evidently higher in I/R group than that in S group and expression of cytochrome C protein was evidently lower than that in S group (p<0.05). The expression of caspase-3 protein was evidently decreased in IPOST group and IPC group and the expression of cytochrome C protein was evidently increased (p<0.05). CONCLUSIONS: IPOST can reduce hepatic apoptosis caused by hepatic ischemia/reperfusion injury in rats, which may be achieved by inhibiting the mitochondria pathway. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Recent researches have proved that long non-coding RNAs (lncRNAs) has an important role in many diseases. In this research, lncRNA AK027294 was explored to identify how it functions in the development of gastric cancer (GC). PATIENTS AND METHODS: Real Time-quantitative- Polymerase Chain Reaction (RT-qPCR) was utilized to detect AK027294 expression in GC patients. Then, MTT assay, colony formation assay, and EdU incorporation assay were performed to identify its function in GC cells. Furthermore, the potential mechanism was also explored using mechanism assays. RESULTS: AK027294 expression level was significantly higher in GC tissue samples and cell lines. Results of MTT assay, colony formation assay, and EdU incorporation assay showed that cell proliferation was inhibited through the silence of AK027294 in GC cells, while cell proliferation was promoted through overexpression of AK027294 in GC cells. Furthermore, the expression of PCNA was downregulated via silence of AK027294 in GC cells, while the expression of PCNA was upregulated via overexpression of AK027294 in GC cells. The correlation analysis showed that PCNA expression was positively correlated with AK027294 expression in GC tissues. CONCLUSIONS: Our results suggest that AK027294 could enhance cell proliferation of GC cells by upregulating PCNA and might be applied as a novel target for therapy of GC. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Recently, long non-coding RNAs (lncRNAs) have attracted much attention for their roles in tumor progression. The aim of this study was to investigate the specific role of lncRNA MNX1-AS1 in the development of gastric cancer (GC), and to explore the underlying mechanism. PATIENTS AND METHODS: MNX1-AS1 expression in both GC cells and tissue samples was detected by Real Time-quantitative Polymerase Chain Reaction (RT-qPCR). Moreover, the relationship between MNX1-AS1 expression and the overall survival rate of GC patients was explored. Furthermore, wound healing assay and transwell assay were conducted. In addition, the underlying mechanism of MNX1-AS1 in GC was explored by performing RT-qPCR and Western blot assay. RESULTS: MNX1-AS1 expression in GC samples was significantly higher than that of the corresponding normal tissues. Meanwhile, MNX1-AS1 expression was associated with the overall survival time of GC patient. Moreover, the migration and invasion of GC cells were markedly promoted after MNX1-AS1 overexpression in vitro. The mRNA and protein expressions of CDKN1A were remarkably down-regulated after MNX1-AS1 overexpression. Furthermore, the expression level of CDKN1A was negatively correlated with the expression of MNX1-AS1 in GC tissues. CONCLUSIONS: Our results suggested that MNX1-AS1 could enhance the metastasis and invasion of GC cells via suppressing CDKN1A. Furthermore, MNX1-AS1 might be a potential therapeutic target for GC. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Evidence has demonstrated that miR-630 is involved in multiple processes in cancer development and progression. However, the exact functions of miR-630 in papillary thyroid carcinoma (PTC) and the underlying mechanisms remain undefined. Therefore, the aims of the present study were to investigate the role and potential mechanism of miR-630 in tumorigenicity of PTC. PATIENTS AND METHODS: Microarrays were used to analyze the differentially expressed miRNAs in PTC tissues. Expression of miR-630 in PTC tissues and cell lines were determined by a qRT-PCR assay. CCK-8 assays, clonogenic survival assays, cell apoptosis analysis, wound healing assays and transwell invasion assays were used to examine the tumorigenesis function of miR-630 in vitro. Protein expression of signaling pathways was determined by using Western blot. RESULTS: We found that miR-630 was significantly downregulated in PTC tissues and cell lines. Overexpression of miR-630 inhibited PTC cell proliferation and induced cell apoptosis via suppressing the expression of caspase-3 and caspase-6. In addition, up-regulation of miR-630 suppressed the migration and invasion in PTC cells by suppressing EMT progress. Mechanistic investigations showed forced miR-660 expression decreased proteins expression of phosphorylation levels in JAK2/STAT3 signaling. CONCLUSIONS: W e fi rstly p rovided t he e vidence that miR-630 displayed a tumor-promotive role in PTC progression through modulating JAK2/STAT3 pathway, and that a potential therapeutic strategy through enhancing miR-630 expression might benefit PTC patients. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To investigate whether lncRNA H19 can regulate NF1 expression through competitive binding to microRNA- 107, thereby participating in the occurrence and development of non-small cell lung cancer (NSCLC). PATIENTS AND METHODS: Expression levels of H19 and NF1 in NSCLC tissues, paracancerous tissues and NSCLC cell lines were detected by quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR). The binding condition of microRNA-107, H19 and NF1 was detected by dual-luciferase reporter gene assay. Corresponding lentiviruses of H19 were constructed. The regulatory effects of H19 on proliferative and migratory abilities of A549 cells were detected by cell counting kit-8 (CCK-8) and transwell assay, respectively. Rescue experiments were conducted to explore the regulatory interaction between H19 and microRNA-107 in A549 cells. RESULTS: H19 and NF1 were highly expressed in NSCLC tissues and NSCLC cell lines (A549 and HCC823) than those of controls. Overexpressed H19 increased proliferative and migratory abilities of A549 cells. Dual-luciferase reporter gene assay demonstrated that H19 regulates NF1 expression through competitive binding to microRNA-107, thereafter participating in NSCLC development. CONCLUSIONS: H19 is highly expressed in NSCLC, which promotes NSCLC development by regulating NF1 via competitive binding to microRNA- 107. [ABSTRACT FROM AUTHOR]