Search

Objective. To investigate the role of nestin in regulating Keap1-nuclear factor erythroid-2-related factor 2 (Nrf2)-heme oxygenase-1-(HO-1-) mediated antioxidant responses in stress and malignant hematopoiesis. Methods. The mRNA of peripheral blood mononuclear cells was extracted from 20 leukemia patients and 20 healthy people who were hospitalized in the Hematology Department of our hospital from September 2020 to December 2021, and the mRNA levels of nestin, Keap1, Nrf2, and HO-1 were detected by real-time- (RT-) PCR. Results. Compared with healthy controls, the mRNA of nestin, Keap1, Nrf2, and HO-1 in peripheral blood mononuclear cells of leukemia patients was significantly upregulated. Conclusion. The occurrence and development of leukemia are closely related to nestin regulating Keap1-Nrf2-Ho-1 signal pathway. Research Significance. This study determined the effect of nestin on the biological behavior of leukemia cells and its possible mechanism and confirmed that nestin may be a marker of tumor and tumor blood vessels. [ABSTRACT FROM AUTHOR]

As the fifth most common cancer in men and the eighth most common cancer in women, hepatocellular carcinoma (HCC) is the leading cause of cancer-related deaths worldwide, with standard chemotherapy and radiation being minimally effective in prolonging survival. Virus hepatitis, particularly HBV and HCV infection is the most prominent risk factor for HCC development. Mammalian target of rapamycin (mTOR) pathway is activated in viral hepatitis and HCC. mTOR inhibitors have been tested successfully in clinical trials for their antineoplastic potency and well tolerability. Treatment with mTOR inhibitor alone or in combination with cytotoxic drugs or targeted therapy drug scan significantly reduces HCC growth and improves clinical outcome, indicating that mTOR inhibition is a promising strategy for the clinical management of HC. [ABSTRACT FROM AUTHOR]

MicroRNAs play significant roles in the development of cancer and may serve as promising therapeutic targets. In our previous work, miR-219-5p was identified as one of the important metastasis-related microRNAs in HCC. Here we demonstrated that miR-219-5p expression was elevated in HCC tissues and was associated with vascular invasion and dismal prognosis. In multivariate analysis, miR-219-5p was identified as an independent prognostic indicator for HCC patients. Functional mechanism analyses showed that miR-219-5p promoted HCC cell proliferation and invasion in in vitro, as well as in vivo, tumor growth and metastasis in nude mice models bearing human HCC tumors. In addition, cadherin 1 (CDH1) was revealed to be a downstream target of miR-219-5p in HCC cells. In conclusion, miR-219-5p promotes tumor growth and metastasis of HCC by regulating CDH1 and can serve as a prognostic marker for HCC patients. [ABSTRACT FROM AUTHOR]

Background and Aim. Aberrant activationof theTGF-𝛽1/Smad pathway contributes to the activation of hepatic stellate cells (HSCs). MicroRNA-195 has been shown to regulate the activation of HSCs.Theaim of this study was to investigate the role of miRNA-195 in HSCs activation. Methods. A liver fibrotic ratmodel induced by diethylnitrosamine was established. Dual luciferase reporter assays were performed to verify that Smad7 was the target of miRNA-195.The expression levels of miR-195, Smad7, and 𝛼-SMAin HSC-T6 transfected, respectively, with miR-195 mimic, inhibitor, or control were measured by qRT-PCR. The protein expression of Smad7 was detected by Western blot analysis. Results. Enhanced miR-195 and decreased Smad7 were observed in diethylnitrosamineinduced liver fibrotic rats (𝑃 < 0.05). Dual luciferase reporter assays showed that the miR-195 mimic significantly suppressed the luciferase activity of a reporter plasmid carrying the binding site of miR-195 on the 3󸀠UTR of Smad7 (𝑃 < 0.05).ThemiR-195 mimics activated HSCs, further elevated miR-195 and 𝛼-SMA (𝑃 < 0.01), and reduced the Smad7 level (𝑃 < 0.05). The miR-195 inhibitors blocked the activation of HSCs, reduced the expression of miR-195 and 𝛼-SMA (𝑃 < 0.01), and upregulated the expression of Smad7 (𝑃 < 0.05). Conclusion. Collectively, we demonstrated that miRNA-195 activated HSCs by targeting Smad7. [ABSTRACT FROM AUTHOR]