Identification of mite-specific eosinophils in the colon of patients with ulcerative colitis.

The pathogenesis of ulcerative colitis (UC) is unclear. House dust mite (HDM) is associated with immune inflammation in the body. This study is designed to identify the association between HDM and UC clinical symptoms. UC patients (n = 86) and non-UC control (NC) subjects (n = 64) were recruited. Colon lavage fluids (CLF) were collected from HDM skin prick test positive patients during colonoscopy, and analyzed by immunological approaches. HDM was detected in fecal samples, which was positively correlated with UC clinical symptoms. HDM-specific eosinophils and Th2 cells were detected in CLF, which could be specifically activated by exposing to HDM in the culture. Direct exposure to HDM induced eosinophil activation in the colon of UC patients. UC patients displayed elevated levels of Th2 cytokines in the serum. UC clinical symptom scores were positively correlated with serum levels of Th2 cytokines. HDM was detected in UC patients' stools, which was positively correlated with UC clinical symptoms. Direct exposure to HDM could trigger eosinophilic activation of the colon.

Evaluating the value of tumor length times width in colorectal adenocarcinoma with different tumor locations.

The T classification, which reflects the vertical growth pattern of the tumor, is one of the most important prognostic factors in colorectal cancer. We aimed to investigate the prognostic value of tumor length and width in patients with colorectal cancer (CRC). A total of 259 patients with stage I-III CRC who underwent curative resection were reevaluated according to tumor location. One-way ANOVA analysis was conducted to investigate the relationship between the tumor length times width (TLTW) and clinical parameters. Univariate and multivariate analyses were conducted to analyze the potential prognostic factors affecting overall survival (OS) of patients with stage I-III CRC. In the entire cohort, the TLTW was analyzed as a continuous variable. The results suggested that TLTW (P = .003) and tumor location (P = .04) could be independent prognostic factors for patients with CRC. In addition, TLTW had an intimate relationship with tumor location (P < 0.001) and differentiation (P = .003). The mean TLTW of the right colon was significantly larger than mean TLTW of the left colon and rectal cancers. However, the mean TLTW of the left colon cancer was similar to that of the rectal cancer TLTW (P > 0.05, not shown). Subgroup analysis of TLTW according to tumor location suggested that TLTW was an independent prognostic factor for patients with right colon cancer (RCC) (P = .007) rather than left colon cancer (LCC) (P = .49) or rectal cancer (P = .16). Kaplan-Meier (K-M) analysis based on tumor location suggested that the survival rate of RCC patients had a distinctly higher trend rate than LCC patients and RECC patients in the long-term rather than in the short-term. TLTW is closely associated with tumor location in CRC. In addition, TLTW may be an independent prognostic factor for patients with RCC.

Suppression of MIR31HG affects the functional properties of thyroid cancer cells depending on the miR-761/MAPK1 axis.

BACKGROUND: Thyroid cancer is the most prevalent endocrine malignancy. Long non-coding RNA (lncRNA) MIR31HG is abnormally expressed in thyroid cancer tissues. However, the precise, critical role of MIR31HG in thyroid cancer development remains unclear. METHODS: MIR31HG, microRNA (miR)-761 and mitogen-activated protein kinase 1 (MAPK1) were quantified by quantitative real-time PCR (qRT-PCR) and immunoblotting. Cell viability, proliferation, apoptosis, invasion and migration abilities were evaluated by MTS, 5-Ethynyl-2'-Deoxyuridine (EdU), flow cytometry, transwell and wound-healing assays, respectively. Dual-luciferase reporter assays were used to validate the direct relationship between miR-761 and MIR31HG or MAPK1. RESULTS: MIR31HG was overexpressed in human thyroid cancer, and its overexpression predicted poor prognosis. Suppression of MIR31HG impeded cell proliferation, invasion and migration, as well as promoted cell apoptosis in vitro, and diminished the growth of xenograft tumors in vivo. Mechanistically, MIR31HG targeted and regulated miR-761. Moreover, miR-761 was identified as a molecular mediator of MIR30HG function in regulating thyroid cancer cell behaviors. MAPK1 was established as a direct and functional target of miR-761 and MAPK1 knockdown phenocopied miR-761 overexpression in impacting thyroid cancer cell behaviors. Furthermore, MIR31HG modulated MAPK1 expression by competitively binding to miR-761 via the shared binding sequence. CONCLUSION: Our findings demonstrate that MIR31HG targets miR-761 to regulate the functional behaviors of thyroid cancer cells by upregulating MAPK1, highlighting a strong rationale for developing MIR31HG as a novel therapeutic target against thyroid cancer.