Our study investigates the clinical phenotypes and outcomes of patients with antisynthetase syndrome with distinct antisynthetase antibodies and highlights the link between the anti-PL7 antibody and RP-ILD.
Background: Cancer is a significant complication contributing to increased mortality in idiopathic inflammatory myopathies (IIMs), and the association between IIMs and cancer has been extensively reported. Myositis-specific autoantibodies (MSAs) can help to stratify patients into more homogeneous groups and may be used as a biomarker for cancer-associated myositis. In this study, we aimed to systematically define the cancer-associated MSAs in IIMs. Methods: Serum from 627 patients with IIMs was tested for MSAs. The cancer risk with different MSAs was estimated by standardized incidence ratio (SIR). Paraneoplastic manifestation, such as the close temporal relationship between myositis onset and cancer diagnoses in patients with different MSAs, was also evaluated. Results: Compared with the general Chinese population, patients with IIMs and anti-transcriptional intermediary factor (TIF1)-γ antibodies (SIR = 17.28, 95% CI 11.94 to 24.14), anti-nuclear matrix protein (NXP2) antibodies (SIR = 8.14, 95% CI 1.63 to 23.86), or anti-SAE1 antibodies (SIR = 12.92, 95% CI 3.23 to 32.94), or who were MSAs-negative (SIR = 3.99, 95% CI 1.96 to 7.14) faced increased risk of cancer. There was no association between specific MSAs subtypes and certain types of cancer. Paraneoplastic manifestations were observed in the patients carrying anti-TIF1-γ, as well as other MSAs. There were no prognostic differences among the patients with cancer-associated myositis (CAM) from different MSAs subgroups. However, in comparison to those with cancer unrelated to myositis, CAM had a worse prognosis, with an age-adjusted and sex-adjusted Cox hazard ratio (HR) of 10.8 (95% CI 1.38-84.5, p = 0.02) for all-cause mortality.
Epigallocatechin-3-gallate (EGCG), the most abundant polyphenol in green tea extract, has been found to have anticancer activities in various types of cancer. However, the underlying mechanisms are not completely clear. In the present study, the effects of EGCG on migration, invasion, angiogenesis and epithelial-mesenchymal transition (EMT) induced by nicotine in A549 non-small cell lung cancer (NSCLC) cells were investigated, and the underlying molecular mechanisms were preliminarily examined. The results showed that different concentrations of EGCG significantly inhibited nicotine-induced migration and invasion. Moreover, EGCG reversed the upregulation of HIF-1α, vascular endothelial growth factor (VEGF), COX-2, p-Akt, p-ERK and vimentin protein levels and the downregulation of p53 and β-catenin protein levels mediated by nicotine in A549 cells, but had no significant effect on their mRNA levels. Furthermore, EGCG markedly inhibited HIF-1α-dependent angiogenesis induced by nicotine in vitro and in vivo, and suppressed HIF-1α and VEGF protein expression induced by nicotine in A549 xenografts of nude mice. Taken together, the results indicated that EGCG inhibited nicotine-induced angiogenesis and EMT, leading to migration and invasion in A549 cells. The results of the present study suggested that EGCG can be developed into a potential agent for the prevention and treatment of smoking-associated NSCLC.
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