Int J Med Sci
-
Background: Neuron specific enolase (NSE) is a specific biomarker for SCLC. However, the biological roles and aberrant expression of NSE in SCLC have not been well illustrated. Methods: The expression of NSE, miR-93-5p and LINC00657 in SCLC tissues and cell lines were detected using real time quantitative PCR (qRT-PCR) or immunohistochemistry. ⋯ LINC00657 and miR-93-5p promoted SCLC cell migration, invasion and EMT by NSE-mediated manner. Conclusion: Overall, our study revealed a novel role of NSE in SCLC. NSE was positively regulated by LINC00657 through competitively interacting with miR-93-5p, which may be potential targets for SCLC patients.
-
Background: It's reported SARS-CoV-2 could transmit via gastrointestinal tract, with or without pulmonary symptoms. However, as far as we know, there is no effective marker to predict the virus discharge in stool and initial gastrointestinal involvement of COVID-19 patients. Aims: We aimed to investigate the likely biomarker predicting virus discharge in stool and initial gastrointestinal involvement of COVID-19, which may assist the clinicians in better preventing COVID-19 spread. ⋯ Patients were divided into tertile groups by circulating lymphocyte count: lymphocyte ≤0.88*10^9/l ( n = 25 ), 0.88*10^9/l -1.2*10^9/l ( n = 28 ), and >1.2*10^9/l ( n = 23 ), respectively. When circulating lymphocyte count increased from 1st tertile to the 2nd and 3rd tertiles, the risk of initial gastrointestinal symptoms decreased by nearly 75% (OR = 0.25, 95% CI: 0.07, 0.98, p = 0.047), 83% (OR = 0.17, 95% CI: 0.05, 0.63, p = 0.008), after adjusting for likely confounders. Conclusions: The circulating lymphocyte count is inversely associated with virus discharge in stool, and the risk of initial gastrointestinal involvement in COVID-19 patients.
-
Observational Study
UHRF2 promotes Hepatocellular Carcinoma Progression by Upregulating ErbB3/Ras/Raf Signaling Pathway.
Emerging evidence revealed that UHRF2 was implicated in a variety of human diseases, especially in cancer. However, the biological function, clinical significance and underly mechanisms of UHRF2 in hepatocellular carcinoma (HCC) is largely unknown. We analyzed the expression of UHRF2 in 371 HCC tissues and 50 para-cancerous tissues of TCGA database. ⋯ Pearson correlation analysis indicated that the expression of UHRF2 was positively correlated with ErbB3 and its downstream targets SOS1, Ras and Raf-1. Furthermore, we found that overexpression of UHRF2 could upregulate the expression of ErbB3, SOS1, Ras and Raf-1. Our findings suggested that UHRF2 might accelerate HCC progression by upregulating ErbB3/Ras/Raf signaling pathway and it might serve as a diagnostic marker and therapeutic target for HCC patients.
-
Background: When an imbalance occurs between the demand and capacity for protein folding, unfolded proteins accumulate in the endoplasmic reticulum (ER) lumen and activate the unfolded protein response (UPR). In addition, unfolded proteins are cleared from the ER lumen for ubiquitination and subsequent cytosolic proteasomal degradation, which is termed as the ER-associated degradation (ERAD) pathway. This study focused on changes in the UPR and ERAD pathways induced by the repeated inhalation anesthetic exposure in Caenorhabditis elegans. ⋯ Conclusion: Repeated isoflurane exposure caused significant ER stress in C. elegans. Following the increase in UPR, the ERAD pathway was disrupted by repeated isoflurane exposure and ubiquitinated proteins was accumulated subsequently. UPR and ERAD pathways are potential modifiable neuroprotection targets against anesthesia-induced neurotoxicity.
-
The pathogenesis of hallux valgus is not clearly understood. However, genetics research about hallux valgus is rare. Therefore, the present study aimed to explore the pathogeny of hallux valgus from the perspective of genetics. ⋯ We found that (1) FGF9 expressed in hallux valgus region bone tissue was significantly higher than normal bone tissue. (2) miR-182 expression levels in hallux valgus region bone tissue were notably lower than those of normal bone tissue. (3) miR-182 could negatively regulate the expression of FGF9 in osteoblasts. (4) FGF9 may enhance osteoblasts proliferation. We have demonstrated that miR-182 promotes the formation of bone by targeting FGF9, implicating an essential role of miR-182 in the etiology of hallux valgus. Moreover, miR-182 might potentially be a therapeutic target for hallux valgus treatment.