Digital economy, innovation factor allocation and industrial structure transformation-A case study of the Yangtze River Delta city cluster in China.

The attainment of regional high-quality development necessitates the critical role of the digital economy in facilitating the transformation of industrial structures. This study intends to investigate the effect of the digital economy on industrial structure transformation from the perspective of innovation factor allocation using a panel dataset of 41 cities in the Yangtze River Delta region for the period from 2011 to 2020. This paper considers four dimensions to measure the level of industrial structure transformation i.e. industrial structure servitization, industrial structure upgradation, service industry structure upgradation and industrial interaction level. The results of the study suggest that the digital economy can significantly improve industrial structure transformation. The results remain consistent even after several robustness checks. Further, the analysis of the mechanism of action shows that the digital economy can promote industrial structure transformation by optimizing the innovation factor allocation. The study provides several policy implications for the digital economy and its role in the promotion of industrial structure transformation.

Matrine suppresses hepatocellular carcinoma tumorigenesis by modulating circ_0055976/miR-1179/lactate dehydrogenase A axis.

BACKGROUND: Matrine has been identified to have anticancer activity in hepatocellular carcinoma (HCC). Circ_0055976 was highly expressed in HCC. Here, we investigated the function and relationship of Matrine and circ_0055976 in HCC tumorigenesis. METHODS: Cell proliferation and invasion were detected using Cell Counting Kit-8, 5-Ethynyl-2'-deoxyuridine (EdU), colony formation and transwell assays, respectively. Cell aerobic glycolysis was evaluated by detecting glucose consumption, lactate production, and the ratios of ATP/ADP. Levels of genes and proteins were detected by quantitative real-time polymerase chain reaction and Western blotting. The target relationship between miR-1179 and circ_0055976 or lactate dehydrogenase A (LDHA) was analyzed by dual-luciferase reporter assay. The mouse xenograft model was established to conduct the in vivo assay. RESULTS: Matrine suppressed HCC cell proliferation, invasion and anaerobic glycolysis in vitro. Circ_0055976 was highly expressed in HCC tissues and cells, and was reduced by Matrine treatment. Moreover, overexpression of circ_0055976 reversed the anticancer effects of Matrine in HCC cells. Mechanistically, circ_0055976/miR-1179/LDHA formed an axis. Circ_0055976 knockdown or miR-1179 overexpression impaired HCC cell proliferation, invasion, and anaerobic glycolysis, which were reversed by miR-1179 inhibition or LDHA overexpression. Meanwhile, forced expression of LDHA abolished the regulatory effects of Matrine on HCC cells. In the clinic, Matrine impeded HCC tumor growth in vivo, and this effect was boosted after circ_0055976 silencing. CONCLUSION: Matrine suppressed HCC cell proliferation, invasion, and anaerobic glycolysis via circ_0055976/miR-1179/LDHA axis, providing a new insight into the clinical application of Matrine in HCC treatment.

Matrine suppresses liver cancer progression and the Warburg effect by regulating the circROBO1/miR-130a-5p/ROBO1 axis.

Matrine, an effective component extracted from the traditional Chinese herb, Sophora flavescens, has been indicated to exert antitumor activity in different types of cancer. However, the role and precise mechanism of matrine in the progression of liver cancer remains largely unclear. Cell viability, cell proliferation, cell apoptosis, and Warburg effect were estimated by cell counting kit-8 assay, colony formation assay, flow cytometry assay, and glucose uptake and lactate production assay, respectively. The candidate Circular RNAs (circRNAs) were screened by integrating the Gene Expression Omnibus database (GSE155949) analysis with the online program GEO2R. A quantitative real-time polymerase chain reaction was employed to test the expression of circRNA circROBO1, microRNA miR-130a-5p, and roundabout homolog 1 (ROBO1). The interaction of circROBO1/miR-130a-5p/ROBO1 axis was predicted and confirmed by bioinformatics analysis, a dual-luciferase reporter assay, and an RNA pull-down assay. A xenograft mouse model was employed to reveal the role of matrine in vivo. Matrine repressed liver cancer cell viability, proliferation, and Warburg effect, but increased cell apoptosis in vitro. CircROBO1 and ROBO1 were upregulated, but miR-130a-5p was downregulated in liver cancer tissues. Additionally, matrine could reduce the expression of circROBO1 and ROBO1, and increase the expression of miR-130a-5p. Mechanically, overexpression of circROBO1 partly recovered the effect of matrine on liver cancer cell viability, proliferation, apoptosis, and Warburg effect by regulating the miR-130a-5p/ROBO1 axis. Matrine impeded liver cancer development by mediating the circROBO1/miR-130a-5p/ROBO1 axis, which provided a theoretical basis for the application of matrine as an effective anticancer drug for liver cancer.

Matrine inhibits hepatocellular carcinoma cell malignancy through the circ_0013290/miR-139-5p/MMP16 pathway.

BACKGROUND: Previous studies have shown the anticancer effect of Matrine on hepatocellular carcinoma (HCC); however, the underlying mechanism is still indistinct. METHODS: The expression of circular RNA_0013290 (circ_0013290), microRNA-139-5p (miR-139-5p), matrix metallopeptidase 16 (MMP16), CyclinD1 and N-cadherin was analyzed by quantitative real-time polymerase chain reaction, Western blotting or immunohistochemistry assay. Cell viability, proliferation, apoptosis, invasion and tube formation were analyzed by cell counting kit-8, 5-Ethynyl-2'-deoxyuridine, flow cytometry analysis, transwell invasion and tube formation assays, respectively. The associations among circ_0013290, miR-139-5p and MMP16 were predicted by starbase online database, and identified by dual-luciferase reporter and RNA pull-down assays. A xenograft mouse model assay was conducted to disclose the effects of circ_0013290 and Matrine on tumor tumorigenesis in vivo. RESULTS: Circ_0013290 and MMP16 expression were significantly upregulated, while miR-139-5p was downregulated in HCC tissues and cells compared with the matched normal liver tissues and cells. Matrine treatment inhibited HCC cell proliferation, invasion and tube formation but induced cell apoptosis, accompanied by the decrease of CyclinD1 and N-cadherin expression; however, these effects were counteracted when circ_0013290 expression was increased. MiR-139-5p depletion or MMP16 introduction relieved Matrine-induced effects in HCC cells. The regulation of circ_0013290 toward HCC cell processes involved MMP16. With respect to the mechanism, circ_0013290 acted as a miR-139-5p sponge, and miR-139-5p targeted MMP16 in HCC cells. Besides, circ_0013290 regulated MMP16 expression through miR-139-5p. Further, circ_0013290 depletion enhanced the inhibitory effects of Matrine on tumor tumorigenesis. CONCLUSION: Matrine inhibited HCC cell malignancy through the circ_0013290/miR-139-5p/MMP16 pathway, suggesting that Matrine is a potential therapeutic agent for HCC.

Semen Brassicae ameliorates hepatic fibrosis by regulating transforming growth factor-ß1/Smad, nuclear factor-κB, and AKT signaling pathways in rats.

PURPOSE: There is no effective treatment for liver fibrosis, which is a common phase during the progression of many chronic liver diseases to cirrhosis. Previous studies found that Semen Brassicae therapy can effectively improve the clinical symptoms of patients with asthma, allergic rhinitis, and chronic lung diseases; however, its effects on liver fibrosis in rats and its possible mechanisms of action remain unclear. METHODS: Rats were injected intraperitoneally with 4% thioacetamide aqueous solution (5 mL·kg-1) at a dose of 200 mg·kg-1 twice a week for 8 consecutive weeks to establish the liver fibrosis model and were then treated with different concentrations of Semen Brassicae extract. After Semen Brassicae treatment, the morphology of the liver tissue was analyzed using hematoxylin and eosin and Masson's trichrome staining, and liver index and liver fibrosis grade were calculated. Thereafter, the levels of collagen-I, collagen-III, α-SMA, transforming growth factor (TGF)-ß1, p-Smad 2/3, Smad 2/3, Smad4, NF-κB-p65, p-NF-κB-p65, IL-1ß, IL-6, AKT, and p-AKT were determined using Western blotting. RESULTS: Compared with the untreated model group, the Semen Brassicae-treated group showed significantly decreased liver function indices; expression levels of collagen-I, collagen-III, and α-SMA; and hepatic fibrosis. Further studies also showed that the expression of TGF-ß1, Smad4, p-Smad 2/3/Smad 2/3, p-NF-κB-p65/NF-κB-p65, IL-1ß, IL-6, and p-AKT/AKT significantly decreased after the treatment. CONCLUSION: These results indicate that Semen Brassicae exhibits an anti-hepatic fibrosis effect, and the underlying mechanism of action may be related to the regulation of TGF-ß1/Smad, NF-κB, and AKT signaling pathways and the reduction of extracellular matrix deposition.