Similar Datasets
Project description:To reveal the HNRNPAB-regulated lncRNAs, we performed microarray analyses to screen differential lncRNAs in HCC cells after stable overexpression or knockdown of HNRNPAB. MHCC97H and HCCLM3 (HCC cell lines with high-metastatic potentials), PLC/PRF/5 and HepG2 (HCC cell lines with low-metastatic potentials) were used in this study. HepG2-control, HepG2-hnRNPAB, PLC/PRF/5-control, PLC/PRF/5-hnRNPAB, MHCC97H-control, MHCC97H-sh-hnRNPAB, HCCLM3-control, HCCLM3-sh-hnRNPAB were perpared with hU6-MCS-CBh-gcGFP-IRES-puromycin-shRNA-HNRNPAB/mock lentiviral and Ubi-MCS-SV40-EGFP-IRES-puromycin-HNRNPAB/mock cDNA lentiviral,respectively, each performed in triplicate.
2019-01-01 | GSE124516 | GEO
Project description:The role and mechanism of CSTF2 in hepatocellular carcinoma are unclear. We constructed CSTF2 knockout HUH7 and PLC/PRF/5 cells to analyze the function of CSTF2 in liver cancer and the downstream gene changes it induces.
2024-02-10 | GSE254649 | GEO
Project description:The proteomic profiling of nine commonly used HCC cell lines Hep3B, HepG2, HepG2.2.15, HUH7, PLC/PRF/5, MHCC97L,MHCC97H,HCCLM3 and HCCLM6
2022-11-11 | PXD036643 | Pride
Project description:Purpose: to analyze gene expression in XL413 treated liver cancer cells. Methods: PLC/PRF/5 cells are treated with XL413 (10uM) for 96 hours .For RNA sequencing, the library was prepared using TruSeq RNA sample prep kit according to the manufacturer’s protocol (Illumina). Gene set enrichment analysis was performed using gene set enrichment analysis software.
2021-09-12 | GSE183751 | GEO
Project description:Effect of PF-429242 on gene expression in liver cancer cells
| PRJNA949152 | ENA
Project description:Gene expression profiling comparisons of HepG2.2.15 or PLC/PRF/5 cells either mock (M) transfected or transfected with 0.2 microM S2 RNA or Scrambled (SCR) siRNA were carried out in duplicate 48 hours after transfection. The experiments were carried out in duplicate (a and b). The following combinations of RNA were used on 2 slides each: 1. 2.2.15 cells: mock transfection (reference) versus S2 treatment (test) 2. 2.2.15 cells: mock transfection (reference) versus Scr treatment (test) 3. 2.2.15 cells: Scr treatment (reference) versus S2 treatment (test) 4. PLC/PRF/5 cells: mock transfection (reference) versus S2 treatment (test) 5. PLC/PRF/5 cells: mock transfection (reference) versus Scr treatment (test) 6. PLC/PRF/5 cells: Scr treatment (reference) versus S2 treatment (test)
2005-11-03 | E-SMDB-2880 | biostudies-arrayexpress
Project description:PF-04287881 induced varying degrees of liver necrosis and phospholipidosis in a 34-inbred strain Mouse Diversity Panel (MDP) study. Four strains with differing susceptibilities to these phenotypes (MA/MyJ, NZW/LacJ, SM/J, WSB/EiJ) were selected for analysis of gene expression changes in the liver. The objective of this study was to identify gene expression changes that drive PF-04287881-induced liver injury.
2016-10-21 | GSE52620 | GEO
Project description:PF-04287881 induced varying degrees of liver necrosis and phospholipidosis in a 34-inbred strain Mouse Diversity Panel (MDP) study. Four strains with differing susceptibilities to these phenotypes (MA/MyJ, NZW/LacJ, SM/J, WSB/EiJ) were selected for analysis of gene expression changes in the liver. The objective of this study was to identify gene expression changes that drive PF-04287881-induced liver injury. Thirty-one total samples were analyzed: N=4 per treatment and strain, except PF-04287881-treated WSB/EiJ (N=3) where one animal died before the completion of the study due to gavage error. Two strains exhibited findings of PF-04287881-induced Kupffer cell vacuolation and were coded as phospholipidosis responders (MA/MyJ and NZW/LacJ). One strain exhibited findings of single cell necrosis and was coded as a necrosis responder (NZW/LacJ).
2016-10-21 | E-GEOD-52620 | biostudies-arrayexpress
Project description:Purpose: Hepatic stellate cell (HSC) and Hydrogen sulfide (H2S) both play important roles in Hepatocellar carcinoma (HCC). Whereas, in the microenvironment of HCC, whether HSC participates in regulating the biological process of HCC cells by releasing H2S remains elusive. In this study, we investigate how activated HSC influence HCC fate. Methods: The effects of LX-2 and H2S on biological functions of HCC cells were analyzed with Flow cytometry and CCK-8. RNA-sequencing, Western blotting, Quantitative real-time reverse transcription PCR (RT-qPCR), siRNA, immunofluorescence and chromatin immunoprecipitation (ChIP) assays were carried out to examine the effect of H2S on JNK/JunB-TNFSF14 (tumor necrosis factor superfamily member 14) signaling pathway. Specimens from HCC patients were analyzed by using RT-qPCR and Western blotting assays for evaluating the expression of TNFSF14. Statistical analysis was used to analyze the correlation between TNFSF14 expression and clinical data of HCC patients. Results: LX-2 cells is able to induce HepG2 and PLC/PRF/5 cells apoptosis by releasing H2S. RNA- sequencing results showed that TNFSF14 gene was changed in both LX-2 and NaHS group. NaHS dosage and time-dependently up-regulated TNFSF14 mRNA and protein expression in both HepG2 and PLC/PRF/5 cells. NaHS treated in HCC cells led to JNK/JunB signaling pathway activating and greater binding of JunB to its responsive elements on TNFSF14 promoter. Impairment of TNFSF14 induction alleviated LX-2 and NaHS induced apoptosis of HepG2 and PLC/PRF/5 cells. Furthermore, mRNA and protein expressions of TNFSF14 in HCC tissues was lower than in the adjacent tissue. HCC patients with low expression of TNFSF14 have higher malignant degree and poor prognosis. Conclusions: Demonstration of the involvement of HSC-derived H2S in JNK/JunB mediated expression of TNFSF14 gene strongly indicates H2S palys an important role in the regulation of HCC apoptosis.
2022-03-22 | GSE193660 | GEO
Project description:The Wilms´ tumor 1 gene (WT1) encodes a transcription factor involved in cell growth and development. As we previously reported WT1 expression is hardly detectable in normal hepatic tissue but is induced in liver cirrhosis. Although WT1 has been found to be overexpressed in a number of malignancies, the role of WT1 in hepatocarcinogenesis has not been clarified. We found that WT1 is expressed in several human hepatocellular carcinoma (HCC) cell lines including PLC/PRF/5 and HepG2, and in HCC tumor tissue in 42% of patients. WT1 small interfering RNAs did not affect proliferation rate of HCC cells but abrogated their resistance to anoikis. Transcriptome analysis of PLC/PRF/5 cells after WT1 knockdown demonstrated upregulation of 251 genes and downregulation of 321. Ninety per cent of the former corresponded to metabolic genes mostly those characterizing the mature hepatocyte phenotype. On the contrary, genes that decreased upon WT1 inhibition were mainly related to defense against apoptosis, cell cycle and tumor progression. In agreement with these findings WT1 expression increased the resistance of liver tumor cells to doxorubicin, a compound used to treat HCC. Interestingly, doxorubicin strongly enhanced WT1 expression in both HCC cells and normal human hepatocytes. Among different chemotherapeutics, induction of WT1 transcription was restricted to topoisomerase 2 inhibitors. When WT1 expression was prohibited doxorubicin caused a marked increase in caspase-3 activation. In conclusion, WT1 is expressed in a substantial proportion of HCC contributing to tumor progression and resistance to chemotherapy, suggesting that WT1 may be an important target for HCC treatment. Keywords: Cell type comparison
2008-10-03 | GSE12886 | GEO