Gastrodin inhibits prostate cancer proliferation by targeting canonical Wnt/ß-catenin signaling pathway.

Prostate cancer is an epithelial malignant tumor occurring in the prostate and is the most common malignant tumor in the male genitourinary system. In recent years, the incidence of prostate cancer in China has shown a trend of sudden increase. The search for new and effective drugs to treat prostate cancer is therefore extremely important.The canonical Wnt/ß-catenin signaling pathway has been shown to be involved in the regulation of tumor proliferation, migration and differentiation. Activation of the canonical Wnt/ß-Catenin signaling pathway in the prostate has oncogenic effects. Drugs targeting the canonical Wnt/ß-catenin signaling pathway have great potential in the treatment of prostate cancer. In this study, we found that Gastrodin could significantly inhibit the proliferation of prostate cancer cell line PC3 and DU145. Oral administration Gastrodin could significantly inhibit the tumor growth of PC3 cells subcutaneously injected. Gastrodin has an inhibitory effect on canonical Wnt/ß-Catenin signaling pathway in Prostate cancer, and this inhibitory effect can be abolished by Wnt/ß-Catenin agonist LiCl. These findings raise the possibility that Gastrodin can be used in the treatment of Prostate cancer by targeting canonical Wnt/ß-Catenin signaling pathway.

Orientin regulates the proliferation and migration of hepatocellular carcinoma cells.

Orientin is a flavone isolated from medicinal plants used in traditional Chinese medicine (TCM) that suppresses the growth of cancer cells in vitro. The effects of orientin in hepatoma carcinoma cells remain unknown. The aim of this paper is to investigate the effects of orientin on the viability, proliferation, and migration of hepatocellular carcinoma cells in vitro. In this study, we found that orientin could inhibit the proliferation, migration, and the activation of NF-κB signaling pathway in hepatocellular carcinoma cells. An activator of NF-κB signaling pathway, PMA, could abolish the inhibitory effect of orientin on NF-κB signaling pathway and proliferation and migration of Huh7 cells. These findings raise the possibility that orientin can be used in the treatment of hepatocellular carcinoma.

TBC1D25 alleviates nonalcoholic steatohepatitis by inhibiting abnormal lipid accumulation and inflammation.

Nonalcoholic fatty liver disease (NAFLD) is a strong stimulant of cardiovascular diseases, affecting one-quarter of the world's population. TBC1 domain family member 25 (TBC1D25) regulates the development of myocardial hypertrophy and cerebral ischemia-reperfusion injury; however, its effect on NAFLD/nonalcoholic steatohepatitis (NASH) has not been reported. In this study, we demonstrated that TBC1D25 expression is upregulated in NASH. TBC1D25 deficiency aggravated hepatic steatosis, inflammation, and fibrosis in NASH. In vitro tests revealed that TBC1D25 overexpression restrained NASH responses. Subsequent mechanistic validation experiments demonstrated that TBC1D25 interfered with NASH progression by inhibiting abnormal lipid accumulation and inflammation. TBC1D25 deficiency significantly promoted NASH occurrence and development. Therefore, TBC1D25 may potentially be used as a clinical therapeutic target for NASH treatment.

The increasing incidence and high body mass index-related burden of gallbladder and biliary diseases-A results from global burden of disease study 2019.

Background: Gallbladder and biliary diseases are common gastrointestinal conditions associated with huge socioeconomic costs and are considered risk factors for cardiovascular diseases and digestive system cancers. The prevalence and incidence of gallbladder and biliary diseases have not received enough attention from 1990 to 2019. Several non-communicable diseases were associated with the incidence of gallbladder and biliary diseases. It is necessary to clarify the change in the incidence and disability burden of gallbladder and biliary diseases worldwide. Methods: Data on high body mass index (BMI)-related disease burden and incidence, years of life lost prematurely, and years lived with disability (YLDs) due to gallbladder and biliary diseases were obtained from the Global Burden of Disease 2019. The estimated annual percentage change was calculated to qualify the gallbladder and biliary disease burden change. Results: The global age-standardized incidence rate has increased from 585.35 per 100,000 (95% UI: 506.05-679.86) in 1990 to 634.32 per 100,000 (95% UI: 540.21-742.93) in 2019. And the increase in incidence was positively correlated with rising high BMI-related summary exposure value. The high BMI-related YLDs of gallbladder and biliary diseases have increased worldwide over time. Globally, the 25-49 age group suffered a rapid rise in incidence and high BMI attributable to the YLDs rate of gallbladder and biliary diseases. Conclusion: The global incidence and high BMI-related YLDs of gallbladder and biliary diseases remain prominent to increase over the past 30 years. Notably, the incidence and high BMI-related YLDs among people aged 25-49 years have rapidly increased over time. Therefore, high BMI should be emphasized in strategic priorities for controlling gallbladder and biliary diseases.

CXCL8 Facilitates the Survival and Paclitaxel-Resistance of Triple-Negative Breast Cancers.

BACKGROUND: This study aimed to demonstrate CXCL8 expression in TNBC tissues and cells, and elucidate the functional mechanism of CXCL8 in paclitaxel (PTX)-resistant TNBC. METHODS: Bioinformatics analysis was performed to identify differentially expressed genes (DEGs) in PTX-resistant TNBC using publicly available data from the GEO, TCGA and METABRIC databases. STRING was used to identify the interacting partners of CXCL8. Kaplan-Meier software was used to analyze the relationship between CXCL8 expression and patient survival rate. The protein expression and distribution of CXCL8 were examined by immunohistochemistry, MTT assay and colony formation assay were performed to determine cell viability of TNBC cells treated with PTX. Western blotting was used to assess the levels of drug resistance and apoptosis-related proteins. GO-KEGG analysis was conducted on the DEGs to identify enriched signaling pathways. RESULTS: The results of bioinformatics analysis demonstrated a high expression of CXCL8 in TNBC tissues and cells. Kaplan-Meier analysis revealed that the expression of CXCL8 is associated with poor prognosis. CXCL8 was upregulated in PTX-resistant TNBC cells. Knockdown of CXCL8 increased the sensitivity of TNBC cells to PTX. Mechanically, CXCL8 deficiency regulated PTX resistance in TNBC cells via cell apoptosis signaling pathway. CONCLUSION: Our work demonstrated that CXCL8 may be a potential molecule to be targeted for the treatment of PTX-resistant TNBC.