Background: OAS1 expression in pancreatic cancer has been confirmed by many studies. However, the prognostic value and mechanism of OAS1 in pancreatic cancer have not been analyzed.Methods: The RNA-seq in pancreatic cancer were obtained by UCSC XENA and GEO database. In addition, immunohistochemical validation and analysis were performed using samples from the 900th hospital. The prognosis of OAS1 was evaluated by timeROC package, Cox regression analysis, and Kaplan-Meier survival curves. Then, the main functional and biological signaling pathways enrichment and its relationship with the abundance of immune cells were analyzed by bioinformatics.Results: OAS1 was highly expressed in pancreatic cancer compared with normal pancreatic tissue. High OAS1 expression was associated with poor overall survival (p<0.05). The OAS1 was significantly correlated to TNM staging (p=0.014). The timeROC analysis showed that the AUC of OAS1 was 0.734 for 3-year OS. In addition, the expression of OAS1 was significantly correlated with the abundance of a variety of immune markers. GSEA showed that enhanced signaling pathways associated with OAS1 include Apoptosis, Notch signaling pathway, and P53 signaling pathway.Conclusions: OAS1 is a valuable prognostic factor in pancreatic cancer. Moreover, it may be a potential immunotherapeutic target.

Objectives During the 2019 Coronavirus disease (COVID-19) outbreak, malnutrition may contribute to COVID-19 adverse outcomes. We conducted a clinical epidemiological analysis to investigate the association of malnutrition with hospitalized duration in patients with COVID-19. Design Retrospective survey study. Setting Taikang Tongji (Wuhan) hospital in Wuhan, China. Participants 139 patients with COVID-19. Methods In total, 139 patients with COVID-19 from patients in the Infection Department of Taikang Tongji (Wuhan) hospital from February 2020 to April 2020 were analyzed retrospectively. We used the “Global leadership Initiative on Malnutrition(GLIM)” assessment standard published in 2019 to assess nutritional status. Prolonged hospitalization was lasting more than the median value of the hospitalized days (17 days) in this population. Results According to the assessment results of GLIM nutrition assessment, the patients were divided into malnutrition group and normal nutrition group. Compared with the patients in the normal nutrition group, the hospitalization time was longer(15.67±6.26 days versus 27.48±5.04 days, P = 0.001). Kaplan-Meier analysis showed patients with malnutrition were more likely to be hospitalized longer compared with those normal nutrition (mean with 95% confidence interval [CI]: 28.91[27.52–30.30] versus 22.78[21.76–23.79], P = 0.001). COX regression analysis showed that malnutrition (hazard ratio [HR] = 3.773, P for trend = 0.001) was proportional associated with being discharged from hospital delayed. Conclusion and implications Present findings suggested that malnutrition contributed to predicting a probability of prolonged hospitalization in patients with COVID-19 infection, to whom extra attentions and precautions should be paid during clinical treatments. Based on the existing results, it is recommended that inpatients with nutritional risk or malnutrition start nutritional support treatment as soon as possible.

Purpose: Early detection and prognostic prediction of hepatocellular carcinoma (HCC) remain a great challenge. In this study, we explored the role and diagnostic significance of stanniocalcin 2 (STC2), recently identified as a secretory protein, in HCC. Methods: STC2 mRNA and protein in HCC tissues were examined by qRT-PCR and immunohistochemistry. The regulatory role of HCC growth by STC2 was evaluated in vitro and in vivo. Serum STC2 levels were determined in HCC patients and compared to those with liver cirrhosis (LC) and normal controls (NC). The difference and significance of STC2 levels between groups were analyzed by Mann–Whitney U-test. The diagnostic value of serum STC2 in detecting early HCC was assayed with receiver operating characteristics (ROC). The association of STC2 with overall survival (OS) was determined with Kaplan–Meier method. Results: STC2 was elevated in about 77.1% HCC patients and correlated with advanced tumor progression. Overexpression or knockdown of STC2 stimulated or suppressed HCC colony formation and xenograft tumor growth. AKT activation played a critical role in tumor-promoting effect of STC2. The median level of serum STC2 in HCC patients (n = 98, 2086.6 ng/L) was 2.6-fold and 4.2-fold that in LC patients (n = 42, 801.9 ng/L) and NC (n = 26, 496.9 ng/L), respectively. A cut-off value 1493 ng/L for STC2 could distinguish early HCC from LC with a sensitivity of 76.9% and a specificity of 76.2%, both of which were superior to AFP at 20 μg/L (sensitivity 69.2%, specificity 52.4%). STC2 was positive in 77.8% (14/18) AFP-negative patients. High STC2 level was correlated with poor overall and disease specific survival. Conclusion: STC2 is upregulated in both tumor and serum of HCC patients, and its overexpression promotes HCC via AKT pathway. STC2 possesses a diagnostic significance and may serve as an auxiliary biomarker of AFP for detecting early HCC.

MiR-34a targeting on Smad4 plays important role in TGF-β1 pathway which is a dominant factor for balancing collagen production and degradation in hepatic stellate cells. TGF-β1/Smad4 regulated collagen deposition is a hallmark of hepatic fibrosis. The potential regulation on miR-34a by LncRNAs in hepatic stellate cells (HSCs) is still reserved to be revealed. In current study, it was hypothesized that a miR-34a interactor, lncRNA CCAT2 may regulate TGF-β1 pathway in liver fibrotic remodeling. The interaction between CCAT2 and miR-34a-5p was checked by dual luciferase assay. the effects of CCAT2 and miR-34a-5p on cell proliferation and apoptosis were verified by MTT assay, colony formation assay, and flow cytometry assay. Dual luciferase activity showed CCAT2 are targets of miR-34a-5p. Sh-CCAT2 transfection prohibit HSCs proliferation and induce HSCs apoptosis, also inhibited ECM protein synthesis in HSCs. Decreased miR-34a-5p enhanced HSCs proliferation, blocked HSCs apoptosis and promoted ECM protein production. miR-34a-5p inhibitor undo protective regulation of sh-CCAT2 in liver fibrosis. Furthermore, clinical investigation showed that CCAT2 and Smad4 expression level were significantly induced, while miR-34a-5p was significantly decreased in HBV related liver fibrosis serum. In conclusion, activated HSCs via TGF-β1/Smad4 signaling pathway was successfully alleviated by CCAT2 inhibition through miR-34a-5p elevation.