Prognostic value of antitumor drug targets prediction using integrated bioinformatic analysis for immunogenic cell death-related lncRNA model based on stomach adenocarcinoma characteristics and tumor immune microenvironment.

Stomach adenocarcinoma (STAD) ranks as the fourth prevalent cause of mortality worldwide due to cancer. The prognosis for those suffering from STAD was bleak. Immunogenic cell death (ICD), a form of induced cellular death that causes an adaptive immune response and has increasing in anticancer treatment. However, it has not been ascertained how ICD-related lncRNAs affect STAD. Using univariate Cox regression and the TCGA database, lncRNAs with prognostic value were identified. Thereafter, we created a prognostic lncRNA-based model using LASSO. Kaplan-Meier assessment, time-dependent receiver operating characteristic (ROC) analyzation, independent prognostic investigation, and nomogram were used to assess model correctness. Additional research included evaluations of the immunological microenvironment, gene set enrichment analyses (GSEA), tumor mutation burdens (TMBs), tumor immune dysfunctions and exclusions (TIDEs), and antitumor compounds IC50 predictions. We found 24 ICD-related lncRNAs with prognostic value via univariate Cox analysis (p < 0.05). Subsequently, a risk model was proposed using five lncRNAs relevant to ICD. The risk signature, correlated with immune cell infiltration, had strong predictive performance. Individuals at low-risk group outlived those at high risk (p < 0.001). An evaluation of the 5-lncRNA risk mode including ROC curves, nomograms, and correction curves confirmed its predictive capability. The findings of functional tests revealed a substantial alteration in immunological conditions and the IC50 sensitivity for the two groups. Using five ICD-related lncRNAs, the authors developed a new risk model for STAD patients that could predict their cumulative overall survival rate and guide their individual treatment.

Predisposition of Inflammatory Bowel Disease Is Influenced by IL-8, IL-10, and IL-18 Polymorphisms: A Meta-Analysis.

BACKGROUND: Whether interleukin (IL)-8, IL-10, and IL-18 polymorphisms influence predisposition of inflammatory bowel disease (IBD) remains uncertain. OBJECTIVES: The authors conducted a meta-analysis to explore relationships between IL-8, IL-10, or IL-18 polymorphisms and predisposition of IBD by merging the results of eligible literatures. METHODS: A thorough literature search in MEDLINE, Embase, Wanfang, VIP, and CNKI was conducted by the authors to identify eligible literatures, and 33 literatures were finally selected for merged analyses. RESULTS: We found that genotypic frequencies of IL-8 rs4073, IL-10 rs1800871, IL-10 rs1800872, and IL-10 rs1800896 polymorphisms among cases with IBD and population-based controls differed significantly. Moreover, we found that genotypic frequencies of IL-8 rs4073, IL-10 rs1800871, and IL-18 rs1946518 polymorphisms among cases with IBD and population-based controls of Asian origin differed significantly, whereas genotypic frequency of IL-10 rs1800896 polymorphism among cases with IBD and population-based controls of Caucasian origin also differed significantly. Furthermore, genotypic frequency of IL-18 rs187238 polymorphism among cases with Crohn's disease (CD) and population-based controls also differed significantly. CONCLUSIONS: The present meta-analysis shows that IL-8 rs4073, IL-10 rs1800871, IL-10 rs1800872, IL-10 rs1800896, and IL-18 rs1946518 polymorphisms may influence predisposition of IBD. Furthermore, IL-18 rs187238 polymorphism may influence predisposition of CD, but not predisposition of ulcerative colitis.

Overexpression of Long Non-Coding RNA FGF14-AS2 Inhibits Colorectal Cancer Proliferation Via the RERG/Ras/ERK Signaling by Sponging microRNA-1288-3p.

Colorectal cancer remains one of most common cancer types with poor prognosis globally. Recent years, numerous studies depicted pivotal roles of lncRNAs in colorectal cancer progression. This study aimed to investigate the role of FGF14-AS2 in colorectal cancer development. FGF14-AS2 was found as a significantly downregulated lncRNA in TCGA dataset. Via RT-qPCR, we confirmed the downregulation of FGF14-AS2 in collected colorectal carcinoma samples. Transfection of plasmid containing full length of FGF14-AS2 repressed cell proliferation and induced elevation of cell apoptosis in colorectal cancer cells. In addition, FGF14-AS2 overexpression inactivated MAPK/ERK signaling in cells. Bioinformatic analysis and subsequent cell-based assays showed that FGF14-AS2 sponging miR-1288-3p, an oncogenic miRNA in colorectal cancer. RERG, the regulator of Ras/ERK pathway, was predicted and verified as target gene of miR-1288. Via downregulation of miR-1288, FGF14-AS2 elevated RERG expression in colorectal cancer cells. Rescue assays indicated that FGF14-AS2 relied on regulation of RERG to control cell proliferation and apoptosis in colorectal cancer. Taken together, the current study demonstrated FGF14-AS2 as a regulator of colorectal cancer development via downregulation of miR-1288-3p and inactivation of Ras/ERK signaling.

The family of apoptosis-stimulating proteins of p53 is dysregulated in colorectal cancer patients.

The apoptosis-stimulating protein of p53 (ASPP) family is a newly identified family protein including ASPP1, ASPP2 and inhibitor of ASPP (iASPP), by which the tumor protein 53 (TP53)-mediated apoptotic process is selectively regulated. Downregulation of ASPP1/ASPP2 and upregulation of iASPP were revealed to be associated with a poor prognosis and metastasis in several types of cancer. However, to the best of our knowledge, the expression of ASPP in colorectal cancer (CRC) has not previously been investigated. The present study analyzed ASPP expression in human CRC tissues with multiple clinical and pathological profiles. A total of 41 patients diagnosed with CRC were enrolled in the present study. The expression of ASPP was detected by immunohistochemistry, immunofluorescence and reverse transcription-quantitative polymerase chain reaction. In addition, the variation in ASPP expression was examined in a number of pathological groups. The associations among ASPP expression, and the expression of TP53, plasma carcinoembryonic antigen (CEA) levels and α-fetoprotein (AFP) levels were also investigated. ASPP1 and ASPP2 expression was significantly reduced, while iASPP expression was elevated in CRC samples compared with expression in adjacent non-cancerous tissues. Downregulation of ASPP1 was detected in the TP53-positive group compared with the TP53-negative group. The increase in iASPP expression was correlated with the grade of malignancy, but not with regional lymph node status or metastases. The expression of ASPP2 was negatively correlated with plasma CEA levels. The results of the present study, not only enrich CRC epidemic and pathological data, but also provide valuable indices for CRC clinical treatment and prognosis.

Assessment of myocardial strain in children with risk factors for atherosclerosis with use of 3D speckle tracking echocardiography.

BACKGROUND: The known risk factors for atherosclerosis such as dyslipidemia, hypertension, obesity, and fasting hyperglycemia are associated with subclinical myocardial dysfunction. We assessed myocardial strain in children who had risk factors for atherosclerosis with use of 3D speckle tracking echocardiography (3DSTE). METHODS: A total of 340 eligible children (mean age [±SD]: 9.5 [±1.9] years; range, 7.1-12.2; 189 males, 151 females). Levels of serum cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), fasting blood glucose (FBG), systolic blood pressure (SBP), diastolic blood pressure (DBP), and body mass index (BMI) were investigated. The parameters of left ventricular (LV) myocardial strain including global longitudinal strain (GLS), global circumferential strain (GCS), and global radial strain (GRS) were measured with use of real time 3DSTE. RESULTS: Left ventricular (LV) global longitudinal strain and global circumferential strain in the groups with isolated dyslipidemia, isolated hypertension, isolated obese/overweight, and combination groups were lower than those in healthy controls (P < .01 for all). Global longitudinal strain (GLS) and GCS showed a negative correlation with the respective risk factors (TG, TC, and LDL-C; SBP and DBP; weight and BMI) (P < .05 for all). Multiple stepwise regression analysis showed a significant negative correlation of GLS and GCS with BMI, TC, TG, and SBP. The degree of myocardial strain aggravated significantly with increase in the number of risk factors in an individual subject.

Hepatic portal venous gas associated with colon cancer: A case report and literature review.

RATIONALE: Hepatic portal venous gas (HPVG) is a very rare radiological finding that occurs when gas enters the portal venous system. HGVG can be caused by various diseases, with the most common being intestinal ischemia or necrosis. While there are few reports of HPVG associated with colon cancer, we report a case of HPVG associated with advanced colon cancer. DIAGNOSIS: The diagnosis of this patient was HPVG caused by colon cancer. INTERVENTIONS: Left colon cancer resection, pancreatic tail resection, splenectomy, and transverse colostomy were performed. OUTCOMES: The patient recovered well, and postoperative paraffin pathology confirmed that the resected tumor was colon cancer. LESSONS: Abdominal computed tomography is an effective method for diagnosing and monitoring HPVG. Klebsiella pneumonia is a potential gas-producing microorganism associated with HPVG, which may be confirmed by Blood culture or drainage culture. The prognosis of HPVG is closely related to the underlying pathology. Surgery should be performed early when there are signs of intestinal ischemia, necrosis, or perforation.