RNA-seq of different genes expression in Hepatocellular Carcinoma cell lines
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE153783 | GEO | 2020/08/03
REPOSITORIES: GEO
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Project description:Abnormal alternative splicing (AS) caused by alterations to splicing factors contributes to tumor progression. Nonetheless, the relevant targets and mechanisms remain elusive in hepatocellular carcinoma (HCC). Here, we reported that overexpression of Ubiquitin-specific protease 39 (USP39), a spliceosome component of the U4/U6.U5 tri-snRNP complex, is associated with poor clinical outcomes and proliferative signaling. Functionally, hepatocyte-specific USP39 knockin mice exhibited enhanced hepatocarcinogenesis. In vitro, USP39 promoted HCC cell proliferation and cell cycle progression in a spliceosome-dependent manner. Transcriptomic analysis revealed that USP39 depletion led to comprehensively impaired constitutive splicing and intriguingly, selective AS of hundreds of genes. USP39-mediated splicing switch of KANK2-S to KANK2-L increased the tumorigenic potential of HCC cells through accelerating KANK2 translation. Mechanistically, USP39 modulates exon inclusion/exclusion via interaction with SRSF6 or hnRNPC in a position-dependent manner. These findings highlight a role for USP39 as a splicing regulator in HCC biology and establishing its position-dependent splicing model.
2023-10-24 | PXD035928 | Pride
Project description:Hepatocellular carcinoma (HCC) ranks sixth among the most common malignancies and fourth in mortality among all kinds of cancers in the world. Recent advances in early diagnosis and therapeutics have led to improved survival of HCC patients, but the recurrence and metastasis are still main reasons for the poor prognosis and high mortality of HCC. Many researches on the mechanism of HCC deterioration have uncovered the epithelial-mesenchymal transition (EMT) as a major trigger for HCC metastasis and invasion.In this study, in order to systematically investigate the dynamic site-specific glycosylation alterations associated with the EMT process of HCC, two hepatoma cell lines SMMC-7721 and HepG2 were treated using HGF and the cell proteins were harvested at six treatment time points. Using TMT-labeling, solid phase extraction and mass spectrometry, we not only detailly profiled N-glycoproteome of both cell lines at site-specific glycosylation level, but also dynamically quantified those intact glycopeptides among six increasing HGF-treated time points. By dynamically quantifying enriched glycopeptides and proteins among six HGF-treated time points in two cell lines, we identified 20 up-regulated intact glycopeptides during the process of EMT, with the majority changed at the glycosylation level instead of protein expression level. The site-specific glycosylation change of those glycoproteins was related to the process of EMT, which was further verified by a series of molecular biology methods, mass spectrometry, and migration and invasion assay in vitro.
2021-09-09 | PXD017033 | Pride
Project description:Sirtuins (SIRT) are NAD-dependent protein deacteylases and function in cellular metabolism, stress resistance, proliferation and disease. For SIRT7, a role in ribosomal gene transcription is proposed, but its function in cancer is currently unknown. In this study, we showed that SIRT7 expression was up-regulated in a large cohort of human hepatocellular carcinoma (HCC) patients, and that high expression of SIRT7 was associated with poor prognosis of HCC patients. Notably, inactivation of SIRT7 by siRNA suppressed tumor cell growth and caused G1/S cell cycle arrest in liver cancer cells. This treatment restored p21WAF1/Cip1 activity, induced Beclin-1 and autophagic gene expression and repressed cyclin D1. To explore mechanisms in SIRT7 regulation, microRNA (miRNA) profiling was carried out. This identified five significantly down-regulated miRNAs in HCC. Bioinformatic analysis of target sites and ectopic expression in HCC cells evidenced miR-125a-5p and miR-125b to suppress SIRT7 and cyclin D1 expression and to induce p21WAF1/Cip1-dependent G1 cell cycle arrest. Furthermore, treatment of HCC cells with 5-aza-2’-deoxycytidine or ectopic expression of wild-type but not mutated p53 restored miR-125a-5p and miR-125b expression and inhibited tumor cell growth to suggest their regulation by promoter methylation and p53 activity. To evidence clinical significance of these findings, mutations in the DNA binding domain of p53 and promoter methylation of miR-125b were investigated. Four out of nine patients with induced SIRT7 carried mutations in p53 gene and one patient showed hypermethylation of miR-125b promoter region. Conclusion: Our findings suggest that oncogenic potential of SIRT in hepatocarcinogenesis and that a regulatory loop is proposed whereby SIRT7 inhibits transcriptional activation of p21WAF1/Cip1 via repression of miR-125a-5p and miR-125b. This makes SIRT7 a promising target in cancer therapy.
2012-09-30 | GSE39678 | GEO
Project description:DNA copy number profiling for all primary tumor samples and HCC cell lines was performed by ROMA, a form of comparative genomic hybridization. The aim was to identify commonly amplifiied and deleted regions across human HCC. 88 primary HCC samples and 12 human HCC cell lines were analyzed.
2011-01-10 | E-GEOD-22916 | biostudies-arrayexpress
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:In this study we investigated the gene expression profiling in three HCC cell lines with different organ-tropism.The parent cell line has low metastasis ability in nude mice model. Subclone 1 has higher metastasis ability specific to lung, and subclone 2 has dual metastasis ability to lung and celiac lymph node. We aimed to explore differentially expressed genes involved in process of HCC metastasis and organ-specific metastasis, and identify their biological functions.
2014-06-30 | GSE38945 | GEO
Project description:High frequency of loss of heterozygosity (LOH) at locus D4S2964 was found in hepatocellular carcinoma (HCC) by our previous studies and others’. The present study was designed to explore genes around the locus affected by LOH and their clinical implications. 440 SNPs located at 49 genes around D4S2964 were selected from NCBI website for the SNPs microarray fabrication. LOH of these SNPs markers in 112 cases of HCC tissues and paired adjacent liver tissues were investigated by the SNP microarray. A map of LOH of SNPs in genes around D4S2964 was constructed. 112 pairs of HCC tissues and corresponding non-tumor tissues was genotyped. LOH and its clinical implication was analyzed.
2015-02-28 | E-GEOD-36277 | biostudies-arrayexpress
Project description:We describe the lncRNA expression profiles of two HCC cell lines, one with high potential for metastasis to the lung (HCCLM3) and the other to lymph nodes (HCCLYM-H2). The HCCLM3(LM3) and HCCLM6 cell lines were derived from the same parental cell line MHCC-97H. LM3 metastasizes to the lung, while HCCLM6 can metastasize to multiple organs in a mouse model. By subcloning HCCLM6, we established the HCCLYM-H2(H2) cell line, which showed stable and high metastatic potential specific to the lymph nodes. In the present study, we compared the expression profiles of HCC cell lines with a similar genetic background but different potential for lung or lymph node metastasis. We found that expression signatures comprising lncRNAs and protein-coding mRNAs were significantly associated with organ-specific HCC metastasis. To further validate microarray data, we selected six lncRNAs (CR613944, BC058547, RP5-1014O16.1, NCRNA00173, lincRNA-CALCA, lincRNA-TSPAN8) and two mRNAs (TSPAN8, CALCB) in the two HCC cell lines using qRT-PCR. Data obtained from qRT-PCR and the microarray was consistent. Differentially expressed lncRNAs between high lymphatic metastatic potential HCC cell H2 and high lung metastatic potiential HCC cell LM3 were identified by microarray and validated using quantitative real-time polymerase chain reaction.
2014-09-03 | E-GEOD-61015 | biostudies-arrayexpress
Project description:In this study we investigated the gene expression profiling in three HCC cell lines with different organ-tropism.The parent cell line has low metastasis ability in nude mice model. Subclone 1 has higher metastasis ability specific to lung, and subclone 2 has dual metastasis ability to lung and celiac lymph node. We aimed to explore differentially expressed genes involved in process of HCC metastasis and organ-specific metastasis, and identify their biological functions. Examination of different gene expression among the 3 cell types.
2014-06-30 | E-GEOD-38945 | biostudies-arrayexpress
Project description:It is known that exosomes (endosome derived vesicles) play important roles in the formation of the tumor microenvironment. Hepatocellular carcinoma (HCC) is a highly malignant cancer, whose malignancy is largely influenced by the tumor microenvironment. The possible role and the specific content of the HCC derived exosomes are however largely unknown. We performed super-SILAC-based mass spectrometry (MS) analyses to interrogate the differential proteins in the exosome of three human HCC cell lines, MHCC97H, MHCCLM3 and Hep3B cells. Exosomal proteins were systematically compared with multi-omics strategies, considering both proteomics and translatomics. With stringent data quality control (quantified unique peptides ≥ 2, FDR ≤ 0.01 at both protein and peptide level), 1907 exosomal proteins were confidently identified from the three HCC cell lines, out of which 469 and 443 exosomal proteins significantly altered in the highly malignant cell lines (MHCC97H/Hep3B and MHCCLM3/Hep3B), respectively. ClueGo and IPA analyses on the differentially expressed proteins (DEPs) revealed that translation and ubiquitination biological processes pathways were significantly more encapsulated in the exosome of higher malignant cell lines. We further observed significantly negative correlation of exosomal protein to cellular protein and translating mRNA in terms of relative abundances comparing the higher malignant cell lines with the low malignant cell line. The negatively correlated genes are also translation regulation-centric. In conclusion, we demonstrated that the exosomal enrichment of translation regulatory proteins is related to the malignant level of HCC cells.
2017-07-18 | PXD004779 | Pride