Project description:We performed whole microarray expressiong prolife of Sk-hep1 cells which could over-express IL-37. This project is to explore the effect of interleukin-37 on hepatocellular carcinoma(HCC) development. We transfected human HCC cell line Sk-hep1 with lentiviral vector encoding IL-37 or control. The successfully transfected cells were sorted by FACS and the cells were further cultured for 24 hours. The cells were harvested and send for microarray analysis.
Project description:To functionally characterize the role of miR-17 family in HCC, lentiviral vector-based miR inhibitor TuD was used to inhibit miR-17 family of microRNAs in HepG2 and SK-Hep1 HCC cell lines
Project description:We observed an increasing trend of nuclear SLC29A2 expression associated with high histological de-differentiation grades, metastasis and poor patient prognosis by immunohistochemical analysis of HCC tumors. Treatments of dipyridamole to SLC29A2 expressing SK-hep1 cells reduced cell viability and cell migration. To examine the anticancer activities of dipyridamole, transcriptome analysis was performed to detect the modulations of oncogenic SLC29A2 and the downstream signaling pathways.
Project description:TARDBP is TARDBP (TDP-43) is a DNA/RNA binding protein and was mutated in human amyotrophic lateral sclerosis (ALS). However, its function in human cancer has not been fully identified, yet.Thus, We carried out microarray to investigate the down-stream target genes of TARDBP after silencing TARDBP in liver cancer cell SK-Hep1. To identify the role of TARDBP in hepatocellular carcinoma cell line, we performed microarray after knocking down TARDBP in hepatocellular carcinoma cell line (3 siLuc, 3 siTARDBP)
Project description:TARDBP is TARDBP (TDP-43) is a DNA/RNA binding protein and was mutated in human amyotrophic lateral sclerosis (ALS). However, its function in human cancer has not been fully identified, yet.Thus, We carried out microarray to investigate the down-stream target genes of TARDBP after silencing TARDBP in liver cancer cell SK-Hep1.
Project description:Hippo signaling pathway is pivotally involved in human cancer. Among the Hippo components, YAP1 is highly active while function of MST1,2 and SAV1 was lost in liver cancer. Based on systematic analysis, we identified KLF5 as YAP1 binding partner in silico. To investigate KLF5 in liver cancer, we performed the gene expression microarray after knocked down YAP1, TEAD1 and KLF5 in SK-Hep1 cell line. To identify the role of YAP1, TEAD1 and KLF5 in hepatocellular carcinoma cell line, we performed microarray after knocking down YAP1, TEAD1 and KLF5 in hepatocellular carcinoma cell line (3 siLuc, 3 siYAP1, 3 siTEAD1, 3 siKLF5)
Project description:Hippo signaling pathway is pivotally involved in human cancer. Among the Hippo components, YAP1 is highly active while function of MST1,2 and SAV1 was lost in liver cancer. Based on systematic analysis, we identified KLF5 as YAP1 binding partner in silico. To investigate KLF5 in liver cancer, we performed the gene expression microarray after knocked down YAP1, TEAD1 and KLF5 in SK-Hep1 cell line.
Project description:Interleukin (IL)-37 suppresses systemic and local inflammation. It is expressed in the epidermis, the external layer of the skin, and is decreased in inflammatory skin diseases including atopic dermatitis (AD) and psoriasis. Therefore, an agent applied topically on the skin that can increase IL-37 could be promising for treating AD and psoriasis; however, the mechanism regulating IL-37 remains largely unknown. Given that IL-37 expression is induced in differentiated keratinocytes, a major component of the epidermis, and that activation of aryl hydrocarbon receptor (AHR), a ligand-activated transcription factor, promotes keratinocyte differentiation, we hypothesized that AHR might be involved in the IL-37 expression in human keratinocytes. We analyzed normal epidermal human keratinocytes (NHEKs) treated with tapinarof and Galactomyces fermentation filtrate (GFF), which are potent AHR modulators. We found that tapinarof and GFF upregulated IL-37 in NHEKs, which was canceled by the knockdown of AHR using siRNA transfection, indicating that AHR mediates IL-37 expression in NHEKs. Furthermore, we found that the knockdown of IL-37 resulted in the upregulation of IL-33, an alarmin cytokine with crucial roles in the pathogenesis of AD and psoriasis. These findings suggest that IL-37 negatively regulates IL-33 expression in NHEKs. Finally, we examined whether tapinarof and GFF treatment modulates IL-33 expression in NHEKs. Such treatment inhibited IL-33 expression, which was partially reversed by the knockdown of either AHR or IL-37. Taken together, our findings provide the first evidence that tapinarof and GFF could have potential to prevent IL-33-overexpressing disorders such as AD and psoriasis via the AHR/IL-37 axis.