Interaction network of Talin-1 in promoting hepatocellular carcinoma progression
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE86062 | GEO | 2016/12/31
SECONDARY ACCESSION(S): PRJNA340158
REPOSITORIES: GEO
Similar Datasets
Project description:Transcriptional profiling of human hepatoellular carcinoma (HCC) cell line: MHCC-97H comparing control untreated MHCC-97H cells with MHCC-97H cells overexpressed ROCK1 protein. Goal was to determine the effect of ROCK1 on global MHCC-97H cell mRNA and lncRNA expression. Transcriptional profiling of human hepatoellular carcinoma (HCC) cell line: MHCC-97H comparing control untreated MHCC-97H cells with MHCC-97H cells overexpressed ROCK2 protein. Goal was to determine the effect of ROCK2 on global MHCC-97H cell mRNA and lncRNA expression. Transcriptional profiling of human hepatoellular carcinoma (HCC) cell line: MHCC-97H comparing MHCC-97H cells overexpressed ROCK1 with MHCC-97H cells overexpressed ROCK2 protein. Goal was to determine the distinction of ROCK1 & 2 on global MHCC-97H cell mRNA and lncRNA expression.
2019-06-19 | GSE122145 | GEO
Project description:Tumor-associated macrophages (TAMs) are crucial components of the tumor microenvironment (TME). They play vital roles in hepatocellular carcinoma (HCC) progression. However, the interactions between TAMs and HCC cells have not been fully characterized. In this study, TAMs were induced using human monocytic cell line THP-1 cells in vitro to investigate their functions in HCC progression. S100 calcium binding protein A9 (S100A9), an inflammatory microenvironment-related secreted protein, was identified to be significantly upregulated in TAMs. S100A9 expression in tumor tissues was associated with poor survival of HCC patients. It could enhance the stem cell-like properties of HepG2 and MHCC-97H cells by activating nuclear factor-kappa B (NF-κB) signaling pathway through advanced glycosylation end-product specific receptor (AGER) in a Ca2+-dependent manner. Furthermore, we found that, after treatment with S100A9, HepG2 and MHCC-97H cells recruited more macrophages via chemokine (C-C Motif) ligand 2 (CCL2), which suggests a positive feedback between TAMs and HCC cells. Taken together, our findings reveal that TAMs could upregulate secreted protein S100A9 and enhance the stem cell-like properties of HCC cells, and provide a potential therapeutic target for combating HCC.
2020-10-23 | GSE158792 | GEO
Project description:Tumor-associated macrophages (TAMs) are crucial components of the tumor microenvironment (TME). They play vital roles in hepatocellular carcinoma (HCC) progression. However, the interactions between TAMs and HCC cells have not been fully characterized. In this study, TAMs were induced using human monocytic cell line THP-1 cells in vitro to investigate their functions in HCC progression. S100 calcium binding protein A9 (S100A9), an inflammatory microenvironment-related secreted protein, was identified to be significantly upregulated in TAMs. S100A9 expression in tumor tissues was associated with poor survival of HCC patients. It could enhance the stem cell-like properties of HepG2 and MHCC-97H cells by activating nuclear factor-kappa B (NF-κB) signaling pathway through advanced glycosylation end-product specific receptor (AGER) in a Ca2+-dependent manner. Furthermore, we found that, after treatment with S100A9, HepG2 and MHCC-97H cells recruited more macrophages infiltration via chemokine (C-C Motif) ligand 2 (CCL2), which suggests a positive feedback between TAMs and HCC cells. Taken together, our findings reveal that TAMs could upregulate S100A9 and enhance the stem cell-like properties of HCC cells, and provide a potential therapeutic target for combating HCC.
2020-10-23 | GSE159264 | GEO
Project description:Background & Aims: Hepatocellular carcinoma (HCC) is the second most lethal cancer due to lack of effective therapies. Although promising, HCC molecular classification, which enriches potential responders to specific therapies, has not yet been assessed in clinical trials of anti-HCC drugs. We aimed to overcome these challenges by developing clinicopathological surrogate indices of HCC molecular classification. Methods: HCC classification defined in our previous transcriptome meta-analysis (S1, S2, and S3 subclasses) was implemented in an FDA-approved diagnostic platform (Elements assay, NanoString). Ninety-six HCC tumors (training set) were assayed to develop molecular subclass-predictive indices based on clinicopathological features, which were independently validated in 99 HCC tumors (validation set). Molecular deregulations associated with the histopathological features were determined by pathway analysis. Sample sizes for HCC clinical trials enriched with specific molecular subclasses were determined. Results: HCC subclass-predictive indices were: steatohepatitic (SH)-HCC variant and immune cell infiltrate for S1 subclass, macrotrabecular/compact pattern, lack of pseudoglandular pattern, and high serum alpha-fetoprotein (>400 ng/mL) for S2 subclass, and microtrabecular pattern, lack of SH-HCC and clear cell variants, and lower histological grade for S3 subclass. Macrotrabecular/compact pattern, a predictor of S2 subclass, was associated with activation of therapeutically targetable oncogene YAP and stemness markers EPCAM/KRT19. BMP4 was associated with pseudoglandular pattern. Subclass-predictive indices-based patient enrichment reduced clinical trial sample sizes from 121, 184, and 53 to 30, 43, and 22 for S1, S2, and S3 subclass-targeting therapies, respectively. Conclusions: HCC molecular subclasses can be enriched by clinicopathological indices tightly associated with deregulation of therapeutically targetable molecular pathways.
2015-06-17 | GSE59548 | GEO
Project description:We performed gene expression profiling of hepatocellular carcinoma (HCC), cholangiocarcinoma (CC), and mixed type of combined HCC and CC (CHC). In comparison of the profiles, a novel class of HCC expressing CC-like traits was identified. Gene expression profiling of 70 hepatocellular carcinoma (HCC), 13 cholangiocarcinoma (CC), and 7 mixed type of combined HCC and CC (CHC) were performed.
2010-06-09 | E-GEOD-15765 | biostudies-arrayexpress
Project description:Patients with Hepatocellular Carcinoma (HCC) and without HCC used for small read cluster identification and small RNA profiling.
2022-06-01 | E-MTAB-8528 | biostudies-arrayexpress
Project description:Hepatocellular carcinoma (HCC) is the most common kind of liver cancer in the world. Portal vein tumor thrombus (PVTT) is one of the most serious complications of HCC and strongly correlated to a poor prognosis for HCC patients. However, the detailed mechanisms of PVTT development still remains to be explored. In this study, we presented the large scale transcriptome analysis of 11 HCC with PVTT patients by RNA-sequencing. The dysregulated genes between HCC and PVTT suggested that the ECM-Receptor Interaction was correlated to the venous metastases of HCC. Among all the recurrent alternative splicing events, we identified exon 6 skipping of RPS24, which is likely to be a cancer driver. We also identified five common fusion genes between HCC and its corresponding PVTT samples, including ARID1A-GPATCH3, MDM1-NUP107, PTGES3-RARG, PRLR-TERT and C9orf3-TMC1. All of the findings broaden our knowledge in PVTT development and may also contribute to the diagnosis and treatment for HCC patients with PVTT.
2015-07-22 | GSE69164 | GEO
Project description:Phosphoinositide 3-kinase (PI3K) signaling, which requires spatial compartmentalization in plasma membrane micro domains, is aberrantly activated in hepatocellular carcinoma (HCC). As a synthetic enzyme of sphingomyelin, sphingomyelin synthase 2 (SMS2) regulates membrane fluidity and microdomain structure. SMS2 functions in various diseases such as atherosclerosis, and diabetes and lung injury. However, the role of SMS2 in HCC tumorigenesis is unclear. In the present study, we found that SMS2 was substantially reduced in tumor tissues and predicted poor prognosis in HCC patients. Function assays in vitro showed that SMS2 could remarkably prevent cell proliferation, cell cycle, cell migration and invasion. Experiments in vivo revealed that SMS2-deficient mice exhibited more severe carcinogenesis and metastasis induced by diethylnitrosamine/carbon tetrachloride. The result of transcriptome sequencing showed that SMS2 was involved in PI3K/Akt signaling pathway. Further study verified that SMS2 could inhibit the expression of PI3K subunit p110α by promoting the ubiquitination of p110α. SMS2 downregulation changed lipid metabolism and PTEN distribution in lipid raft, attenuated p85α-PTEN interaction, thus promoting p85α-p110α interaction. Finally, we found that loss of SMS2 could inhibiting PTEN localization in lipid rafts. The tumor suppression effect of SMS2 on HCC cells could be rescued by p110α expression. Taken together, our findings not only demonstrates that SMS2 is a prospective tumor suppressor and prognosis indicator in HCC, but also provide understanding of the molecular mechanisms by which PI3K/AKT signaling is activated.
2023-05-26 | GSE204898 | GEO
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:Hepatocellular adenomas (HCA) are rare benign tumors that constitute a heterogeneous entity, divided into 5 groups based on molecular features (1) H-HCA with inactivating mutations of Hepatocyte Nuclear Factor 1A (HNF1α), (2) inflammatory HCA (IHCA) with diverse mutations activating the JAK/STAT pathway, (3) b-HCA with activating β-catenin mutation (4) recently identified sh-HCA presenting a Sonic Hedgehog pathway activation and finally, (5) the unclassified HCA (UHCA)). Risk of bleeding of sh-HCA and UHCA is their main clinical feature with malignant transformation. Nowadays, no specific biomarker exists to evaluate this hemorrhage risk. The objective of this study was to combine laser microdissection and mass spectrometry analysis to define Hepatocellular Adenoma proteome in the purpose of identifying specific biomarkers able to predict this bleeding risk.
2018-03-14 | PXD005571 | Pride