Gene expression profiling of Huh-7 cells tranfected NC or DEPDC1 siRNA
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE122124 | GEO | 2018/11/06
REPOSITORIES: GEO
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Project description:Gene expression profiling of Huh-7 cells tranfected NC or DEPDC1 siRNA
| PRJNA503675 | ENA
Project description:Sorafenib, lenvatinib and regorafenib, the multi-RTK inhibitors with potent anti-angiogenesis effects, are currently therapeutic drugs generally recommended for the patients with advanced hepatocellular carcinoma (HCC). To date, however, there have been no published studies on the mechanism underling differential effects of the three drugs on HCC cell proliferation, and the proteomic analysis in HCC cell lines treated by regorafenib or lenvatinib.The present project for the first time performed a direct comparison of their pharmacological interventions for influencing whole cell proteomics using tandem mass tag-based peptide-labeling technique.
2022-10-13 | PXD034073 | Pride
Project description:The expression profiling of HBV-transfected Huh-7 cells and control cells. Hepatocellular carcinoma (HCC) is one of major malignant disease worldwide, and patients with chronic hepatitis B virus (HBV) infection have a high risk of developing HCC. Via microarray gene expression analysis, we detected the gene alteration in HBV transfected hepatoma cells.
2016-06-18 | GSE83489 | GEO
Project description:The diversity and complexity of the cancer transcriptome hold the potential to yield tumor-specific transcripts (TSTs) in cancer. We report a novel LIN28B variant, LIN28B-TST, which is specifically expressed in hepatocellular carcinoma (HCC) and many other cancer types. LIN28B-TST initiates from a de novo alternative transcription initiation site. We found that LIN28B-TST was expressed in HuH-7 HCC cells and NCI-H1299 lung cancer cells, while wild-type LIN28B (LIN28B-WT) was expressed in HEK-293T human embryo kidney cells.
2018-01-24 | GSE109528 | GEO
Project description:Increased ?-fetoprotein (AFP) levels have been reported to predict a poor prognosis in hepatocellular carcinoma (HCC). We assessed the mechanism of AFP involvement in the progression of HCC and determined whether AFP could be a molecular target. We used human HCC cell lines to assess proliferation and apoptosis response to exogenous AFP. We introduced AFP small interfering RNA (siRNA) into HCC cell lines to examine whether it could inhibit cell proliferation and anti-apoptotic properties. The effects of systemically introduced AFP siRNA were assessed using a tumor xenotransplantation model. The effects of AFP on gene expression in HCC cell lines and human HCC specimens were examined. Exogenous AFP induced cell proliferation dose-dependently and inhibited apoptosis induced by 5-fluorouracil (5-FU) in all cell lines examined. AFP siRNA inhibited the proliferation of AFP-producing HCC cell lines and induced apoptosis in co-cultures with 5-FU. Tumor sizes in mice treated with AFP siRNA were significantly smaller than those in controls. AFP siRNA administration in mice induced a low proliferation index and a high apoptosis index in tumors. cDNA microarray analysis, reverse transcription-polymerase chain reaction (RT-PCR), and Western blot using HepG2 and HLE cells with AFP showed that AFP reduced expression of genes related to apoptosis (DFFB) and tumor suppression (NDRG2). Expression of these molecules was also suppressed in human HCC tissues that overexpress AFP. AFP is not only a passive tumor marker, but also an active tumor stimulator through several mechanisms. AFP siRNA introduction may be of possible therapeutic use for HCC. Keywords: Genetic modification Two-condition experiment, Control vs. AFP-stimulated cells.
2008-12-30 | E-GEOD-12307 | biostudies-arrayexpress
Project description:Endothelial cells are critical for angiogenesis, and microRNAs plays important roles in this process. We investigated the regulatory role of microRNAs in endothelial cells of hepatocellular carcinoma (HCC) by examining the microRNA expression profile of human umbilical vein endothelial cells (HUVECs) in the absence or presence of human HCC cells, and identified miR-146a as the most highly up-regulated microRNA. Furthermore, we revealed that miR-146a promoted the expression of platelet-derived growth factor receptor (PDGFRA) in HUVECs, and this process was mediated by BRCA1. Overexpression of PDGFRA in the ECs of HCC tissues was associated with microvascular invasion, and predicted a poorer prognosis. These results suggest that MiR-146a plays a key role in regulating the angiogenic activity of ECs in HCC through miR-146a-BRCA1-PDGFRA pathway. MiR-146a may emerge as a potential anti-angiogenic target on ECs for HCC therapy. We have employed whole genome OneArray to examine the genome expression changes of HUVECs overexpressing miR-146a.
2013-04-13 | E-GEOD-46022 | biostudies-arrayexpress
Project description:To clarify the molecular mechanism by which FNDC4 promotes HCC invasion, mass spectrometry (MS) analysis was performed on the lysates of Huh-7-overexpressing FNDC4 and normal Huh-7 cells.
2022-02-17 | PXD025623 | Pride
Project description:Hepatectomy generally offers the best chance of long-term survival for patients with hepatocellular carcinoma (HCC). Many studies have shown that hepatectomy accelerates tumor metastasis, but the mechanism remains unclear. In this study, palliative hepatectomy was performed in an orthotopic nude mice model of HCC (MHCC97H) with high metastatic potential. Using Human Tumor Metastasis Microarray, we screened the metastasis-related genes in tumor tissues following palliative resection, and found that Metastasis suppressor 1 (MTSS1) located in the central position of gene function net of residual HCC; MTSS1 was up-regulated in residual tumor after palliative resection. Further studies found that MTSS1 enhanced the metastasis of residual HCC. In hepatitis B-related HCC patients undergone palliative hepatectomy, those with higher MTSS1 mRNA expression accompanied by the activation of matrix metalloproteinase 2 (MMP2) in residual HCC, had earlier residual HCC detection after hepatectomy and poorer survival when compared to those with lower MTSS1 level. In different cell lines, the levels of MTSS1 mRNA increased in parallel with metastatic potential. MTSS1 down regulation via siRNA decreased MMP2 activity, reduced invasive potentials of HCC by 28.9% in vitro, and averted the deteriorated lung metastatic extent in vivo. In conclusion, the poor prognosis of hepatitis B-related HCC patients following palliative hepatectomy associates with elevated MTSS1 mRNA expression; therefore, MTSS1 may provide a new research field for HCC diagnosis and treatment.
2015-12-15 | GSE75965 | GEO
Project description:Metformin is a kind of widely used antidiabetic agent, which regulates glucose homeostasis through inhibiting liver glucose production and increasing glucose uptake in muscle. Recent studies suggest that metformin exhibits anticancer properties in a variety of cancers. Although several antitumor mechanisms have been proposed for metformin action, its mode of action in human liver cancer remains not elucidated. In our study we investigated the underlying molecular mechanisms of metformin’s antitumor effect on Huh-7 cells of hepatocellular carcinoma (HCC) in vitro. RNA sequencing (RNA-seq) was performed to explore the effect of metformin on the transcriptome of Huh-7 cells. The results revealed that 4518 genes (with log2 fold change>1 or < -1, p-adjusted value<0.05) were differentially expressed in Huh-7 cells with treatment of 25mM metformin compared to 0mM metformin including 1812 up-regulated and 2706 down-regulated genes. Gene ontology and KEGG pathway analyses identified 54 classical pathways which were significantly enriched, and 16 pathways are closely associated with cancer, such as cell cycle, DNA replication, ECM-receptor interaction and so on. We selected 11 differentially expressed genes, which are closely associated with HCC to validate their differential expressions through quantitative real-time reverse transcription PCR (qRT-PCR). The result exhibited that the genes of FASN, MCM6, MCM5, MARCKS, FADS2, CXCL1, BMP4, SKP2, KNG1, PCNA were down-regulated and DUSP1 is significantly up-regulated in Huh-7 cells with treatment of 25mM metformin. These differentially expressed genes and pathways might play a crucial part in the antitumor effect of metformin, and might be potential targets of metformin treating HCC. Further investigations are required to evaluate the metformin mechanisms of anti-cancer action in vivo.
2021-12-05 | GSE190076 | GEO
Project description:Hepatocellular carcinoma (HCC) is the first cause of death in cirrhotic patients. Liver cirrhosis at a high risk of HCC has abnormal S-Adenosylmethionine (SAMe) levels. Catabolism of SAMe is mainly mediated by Glycine N-methyltransferase (GNMT), Lack in GNMT expression leads to epigenetic regulation of critical carcinogenesis pathways and mounting evidence assigns an essential role of GNMT in HCC. Methods: Here we have studied the role of LKB1-AMPK and RAS in the proliferation and transformation of GNMT-deficient HCC. Results. GNMT-deficient HCC was characterized by LKB1-AMPK misconnection, leading to resistance of apoptosis response mediated by a positive regulation of cAMP-PKA-CaMKKM-NM-2 cascade. Additionally, Ras-mediated hyperactivation of LKB1 contributes to the proliferation of GNMT-deficient HCC in an ERK/p90RSK-dependent manner. The observed LKB1-induced Ras activation, was due to the regulation of RASGRP3 expression. Notably, the human HCC tumors with poorer prognosis showed the lowest levels of GNMT, p-AMPKM-NM-1(Thr172) and the highest activation of Ras/LKB1/RASGRP3 axis. The present data suggest a correlation between LKB1 and RAS activity in a context of HCC with low GNMT expression, indicating that activation of the RAS/LKB1/RASGRP3 cascade might possess an important prognostic role in human liver cancer. Furthermore, these findings open the possibility to design new therapeutic strategies for the treatment of liver cancer. HCC induced wild-type or Gnmt knockout mice at 3 weeks old were used for RNA extraction and hybridization on Illumina microarrays. The study comprises three groups of samples: OKER cell line(n=3), GNMT-KO mouse hepatocytes (n=3) ,GNMT-WT mouse hepatocytes(n=3)
2012-06-30 | E-GEOD-34838 | biostudies-arrayexpress