Scoparone is a biologically active constituent isolated from Artemisia capillaris and possesses a variety of pharmacological activities, such as anti-inflammatory, anti-tumor, anti-allergic and anti-cardiovascular activities. However, there are no studies focusing on the effects of scoparone against cardiac fibrosis. Therefore, the aim of this study was to investigate the effects of scoparone on Angiotensin II (Ang II)-induced extracellular matrix (ECM) remodeling and its possible mechanism in cardiac fibroblasts (CFs). Our results demonstrated that scoparone effectively attenuated CFs proliferation in Ang II-stimulated CFs. Scoparone also prevented the differentiation of CFs to myofibroblasts and ECM proteins (type I collagen and fibronectin) expression in Ang II-stimulated CFs. Furthermore, scoparone prevented Ang II-induced the activation of TGF-β1/Smad signalling in CFs. Taken together, these studies indicated that scoparone attenuated Ang II-induced ECM remodeling in CFs, at least in part, by inhibiting TGF-β1/Smad signalling. These findings suggest that scoparone may be used a novel therapeutic agent against cardiac fibrosis.

Objectives: This study aims to investigate the diagnostic and prognostic values of EpCAM, TGM2, and HE4 in endometrial cancer (EC). Methods: In this study, 42 patients diagnosed with EC (EC group), 41 patients diagnosed with myoma (benign group), and 43 healthy women (healthy group), who applied to Affiliated Hospital of Xuzhou Medical University between March 2018-September 2019 were recruited. Serum EpCAM, TGM2, and IL-33 levels were measured by ELISA, while serum HE4 and CA-125 levels were measured by ECLIA. The serum markers listed above were also measured in 12 paired pre-and post-operative EC patients. The diagnostic and prognostic values of serum markers were analyzed. Results: The serum EpCAM, TGM2, HE4, CA-125, and IL-33 levels were significantly higher in the EC group. The sensitivity and specificity of combined detection of EpCAM and HE4 was 92.86 and 69.05%, which were significantly higher than using a single marker or other combinations. Among these markers, serum HE4 levels were significantly higher in patients with myometrial invasion, metastasis, and lymphovascular invasion (p = 0.006, p = 0.0004, p = 0.0004, respectively). And serum TGM2 levels were significantly decreased in post-operative than that of pre-operative EC patients (p < 0.001). Conclusions: The combination of EpCAM and HE4 showed the highest specificity and sensitivity in the diagnosis of EC. HE4 was successful in the detection of high-risk individuals preoperatively. Additionally, TGM2 might be a prognostic factor for EC.

Glioblastoma multiforme (GBM) is a highly proliferative cancer with generally poor prognosis and accumulating evidence has highlighted the potential of long noncoding RNAs (lncRNAs) in the biological behaviors of glioma cells. This study focused on the identification of lncRNAs to identify targets for possible GBM prognosis. Microarray expression profiling found that 1,759 lncRNAs and 3,026 messenger RNAs (mRNAs) were upregulated, and 1932s lncRNA and 2,979 mRNAs were downregulated in GBM. Bioinformatics analysis and experimental verification identified TCONS_00020456 (TCON) for further analysis. In situ hybridization, along with immunohistochemical and receiver operating characteristic analysis determined TCON (truncation value = 3.5) as highly sensitive and specific in GBM. Grade IV patients with glioma life span with different lncRNA staining scores were analyzed. TCON staining scores below 3.5 indicated poor prognosis (life span ranging from 0.25 to 7 months), even if the glioma was surgically removed. TCON decreased significantly in GBM, and showed a coexpressional relationship with Smad2 and protein kinase C α (PKCα). Overexpression of TCON reduced the proliferation on one hand and migration, invasion on the other. TCON also inhibited epithelial–mesenchymal transformation and glioma progression in vivo, based on a nude mouse tumorigenicity assay. In addition, we predicted a potential binding site and intersection that microRNAs targeting Smad2, PKCα, and TCON through RACE pretest and bioinformatics analysis. Taken together, TCON, regarded as oncosuppressor, targeting the Smad2/PKCα axis plays a novel role in inhibiting the malignant progression of glioma. Moreover, it also demonstrates that the level of TCON can be used as a prognostic and diagnostic biomarker for GBM.

Ovarian cancer is one of the most common gynecological malignancies in women worldwide with a poor survival rate. Cinnamaldehyde (CA), a bioactive substance isolated from cinnamon bark, is a natural drug and has shown that it can inhibit the progression of other tumors. However, the role of CA in ovarian cancer and its mechanism is poorly understood. In this study, wound healing assays, plate cloning, CCK-8, and transwell assays were used to determine cell proliferation and invasion. Western blot and flow cytometry were used to detect apoptosis levels. Western blot and immunofluorescence were used to detect changes in cellular EMT levels. The Western blot was used to detect levels of the PI3K/AKT signaling pathway. In vivo, we established a subcutaneous transplantation tumor model in nude mice to verify the role of CA in the progression and metastasis of ovarian cancer. Our data showed that in vitro CA was able to inhibit the cell viability of ovarian cancer. The results of scratch assay and transwell assay also showed that CA inhibited the proliferation and invasion ability of A2780 and SKOV3 cells. In addition, CA promoted apoptosis by increasing the expression of cleaved-PARP and cleaved-caspase 3 in ovarian cancer cells. Mechanistically, we found that CA inhibited the EGF-induced PI3K/AKT signaling pathway and reduced the phosphorylation levels of mTOR, PI3K, and AKT. The EGF-induced EMT process was also abolished by CA. The EMT process induced by AKT-specific activator SC79 was also suppressed by CA. Furthermore, in in vivo, CA significantly repressed the progression of ovarian cancer as well as liver metastasis. In all, our results suggest that CA inhibits ovarian cancer progression and metastasis in vivo and in vitro and inhibits EGF-induced EMT processes through the PI3K/AKT signaling pathway.

Background Published data have reported the relationships between MTHFR A1298C polymorphisms and cervical cancer susceptibility. However, the conclusions of these findings lack consistency.Methods A comprehensive literature search was performed using Web of Science, PubMed, EMBASE, Cochrane library, Wan Fang and CNKI databases. The pooled odds ratios (ORs) with 95% confidence intervals (CIs) were used to evaluate the correlation of MTHFR A1298C polymorphism and cervical cancer risk. Fixed-effects or random effects models was adopted according to heterogeneity test.Results A total of nine studies (1145 cases and 1690 controls) were included in this meta-analysis. Pooled data revealed that MTHFR A1298C polymorphism was significantly associated with an increased risk of cervical cancer in the allele model (P=0.028); the recessive model (P=0.028); and the heterozygous model (P=0.031).Conclusions Our results revealed that MTHFR A1298C polymorphism was associated with risk of cervical cancer.