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Unknown,Transcriptomics,Genomics,Proteomics

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SM5-1-conjugated gold nanoparticles for antibody therapy in hepatocellular carcinoma

ABSTRACT: As a humanized mouse antibody, SM5-1 can target a membrane protein of about 230kDa over-expressed in hepatocellular carcinoma (HCC), melanoma and breast cancer and it has been found to inhibit the progress of tumor cells. In this study, SM5-1 conjugated gold nanoparticles were prepared to study the antitumor efficacy in the treatment of HCC-LM3-fLuc tumor. The results showed that AU-SM5-1 could inhibit HCC-LM3 hepatocellular carcinoma cell proliferation up to 71.26% at the concentration of 0.5mg/ml contrast with SM5-1 and gold nanoparticles. In order to address the mechanism of the antiproliferative effects of AU-SM5-1, we examined the gene expression in HCC-LM3-fLuc tumor cells based on gene-chip screening. The gene chip results showed that some cycle-related and reactive oxygen species (ROS) related genes including up-regulated P21 and down-regulated duox2 and nox1 genes which were validated by real-time quantitative polymerase chain reaction (PCR).

ORGANISM(S): Homo sapiens

SUBMITTER: ma bo

PROVIDER: E-GEOD-59284 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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SM5-1-conjugated gold nanoparticles for antibody therapy in hepatocellular carcinoma

Project description:As a humanized mouse antibody, SM5-1 can target a membrane protein of about 230kDa over-expressed in hepatocellular carcinoma (HCC), melanoma and breast cancer and it has been found to inhibit the progress of tumor cells. In this study, SM5-1 conjugated gold nanoparticles were prepared to study the antitumor efficacy in the treatment of HCC-LM3-fLuc tumor. The results showed that AU-SM5-1 could inhibit HCC-LM3 hepatocellular carcinoma cell proliferation up to 71.26% at the concentration of 0.5mg/ml contrast with SM5-1 and gold nanoparticles. In order to address the mechanism of the antiproliferative effects of AU-SM5-1, we examined the gene expression in HCC-LM3-fLuc tumor cells based on gene-chip screening.

2014-07-11 | GSE59284 | GEO

STRT RNAseq of THP-1 monocytic cells exposed to surface modified-gold nanoparticles

Project description:Transcriptome comparison to assess the responses of human monocytic cells (THP-1) to gold-nanoparticles (Au-NPs) of two different diameter sizes (5 or 20 nm) with different surface functional groups, i.e., alkylammonium bromide, alkyl sodium carboxylate, or poly(ethylene glycol) (PEG)-terminated thiolate Au-NPs.

2019-06-04 | E-MTAB-7093 | biostudies-arrayexpress

Proteomics study of THP-1 monocytic cells exposed to surface modified-gold nanoparticles

Project description:A proteome comparison was performed to assess the responses of human monocytic cells (THP-1) to gold-nanoparticles (Au-NPs) of two different diameter sizes (5 or 20 nm) with different surface functional groups, i.e., alkylammonium bromide, alkyl sodium carboxylate, or poly(ethylene glycol) (PEG)-terminated thiolate Au-NPs.

2019-03-18 | PXD010858 | Pride

Gold induction of C. metallidurans CH34

Project description:Whole-genome expression microarray experiments were conducted to assess the response of C. metallidurans CH34 to aqueous Au(III)-chloride and identify possible biochemical pathways for Au detoxification. Four microarray experiments were conducted to assess gold response at low, medium and high Au(III)-chloride concentrations (i.e., 10, 50 and 100 ÂµM Au(III)-chloride) and different induction times (10 and 30 minutes with 50 ÂµM Au(III)-chloride). Based on these arrays, the differentially expressed genes upon gold-exposure can be identified. The four microarray experiments (10, 50 and 100 ÂµM Au(III)-chloride at 10 minutes and 50 ÂµM Au(III)-chloride at 30 minutes) were all performed in biological triplicate and containing three (in-slide) technical repeats. For all conditions, the metal-induced sample (Cy5) was compared with the non-induced sample (Cy5) to identify those genes that were differentially expressed upon gold exposure.

2010-06-20 | E-GEOD-14049 | biostudies-arrayexpress

Differential miRNA expression profiles betweenHBV-related HCC tumor versus non-tumor liver tissue

Project description:miRNA played an important role in the process of carcinogenesis in HBV related hepatocellular carcinoma. Therefore, we performed miRNA microarray to evaluate the miRNAs that expressed differentially between HCC tumor versus non-tumor liver tissues. RNA was extracted from snap fresh tissue collected from resected HCC tumor and adjacent non-tumor liver tissues. All HCC tumors were HBV-associated HCC.

2015-07-22 | E-GEOD-69580 | biostudies-arrayexpress

Identification of p53-regulated microRNAs in Hapatocellular Carcinoma (HCC).

Project description:p53 suppresses tumor progression and metastasis by regulating a large set of genes and microRNAs. By profiling 92 primary hepatocellular carcinomas (HCCs) and 9 HCC cell lines, we found that p53 upregulates microRNAs including miR-200 and miR-192 family members. By sequencing TP53 in 92 HCC samples, we classified the 92 samples into two groups (wt and mut). We also classified 9 HCC cell lines by testing p21 expression after DNA-damage mediated p53 activation. We then profiled microRNA expression in 92 HCC tissue samples and 9 HCC celll lines to identify p53-regulated microRNAs.

2011-05-11 | E-GEOD-28661 | biostudies-arrayexpress

Gene expression profiling of effect of Yap inhibition in a genetically engineered mouse model of hepatocellular carcinoma

Project description:Defective Hippo/YAP signaling in the liver results in tissue overgrowth and development of hepatocellular carcinoma (HCC). Here, we uncover mechanisms of YAP-mediated hepatocyte reprogramming and HCC pathogenesis. We show that YAP functions as a rheostat maintaining metabolic specialization, differentiation and quiescence within the hepatocyte compartment. Importantly, treatment with siRNA-lipid nanoparticles (siRNA-LNPs) targeting YAP restores hepatocyte differentiation and causes pronounced tumor regression in a genetically engineered mouse HCC model (mice with liver-specific Mst1/Mst2 double knockout). Furthermore, YAP targets are enriched in an aggressive human HCC subtype characterized by a proliferative signature and absence of CTNNB1 mutations. Thus, our work reveals Hippo signaling as a key regulator of positional identity of hepatocytes, supports targeting YAP using siRNA-LNPs as a paradigm of differentiation-based therapy, and identifies an HCC subtype potentially responsive to this approach. Mice with liver-specific Mst1/Mst2 double-knockout (Adeno-Cre injected Mst1-/-; Mst2Flox/Flox mice) were monitored for the formation of HCC by ultrasound imaging. Animals were then randomized to be treated by intravenous injection of either siYap-LNPs or siLuciferase-LNPs for a period of 9 days.

2015-03-07 | E-GEOD-65665 | biostudies-arrayexpress

Detecting Proteins Glycosylation by a Homogeneous Reac-tion System with Zwitterionic Gold Nanoclusters

Project description:Homogeneous gold nanoclusters (Au NCs) have been widely utilized in drug delivery, chemical sensing, bioassays and bio-labeling due to their unique physical and chemical properties. However, few attentions have been paid on their application in detecting protein post-translational modifications. Herein, we developed a homogeneous reaction system with water-soluble zwitterionic Au NCs to capture glycopeptides from the complex biological samples for the first time. The unique characteristics of Au NCs, such as the molecular-like property, the excellent homogeneity in aqueous solution and organic solvent responsive precipitation, the easy preparation in only 4.5 hours, contribute to the high efficiency and high through-put for capturing the targeted glycopeptides. Briefly, the Au NCs and tryptic protein samples were incubated together in a homogeneous aqueous solution and then the glycopeptides were collected by co-precipitation with zwitterionic Au NCs dur-ing gradually dropping addition of acetonitrile. Compared with the conventional heterogeneous system with solid-state ad-sorbents, the number of characterized glycosylation sites was improved 35%. Finally, the MS detection limitation as low as 50 amol was achieved for the tryptic digests of standard glycoprotein (IgG) and 1576 glycosylation sites from 713 glycopro-teins were feasibly identified from only 60 μg mouse liver proteins

2017-03-29 | PXD005635 | Pride

Broad-spectrum kinome profiling identifies CDK6 upregulation as a driver of lenvatinib resistance in hepatocellular carcinoma

Project description:Lenvatinib is the FDA-approved targeted drug for advanced hepatocellular carcinoma (HCC), but the efficacy is modest due to drug resistance. Tumor kinome re-wiring governs drug resistance in resistant cancer cells, which is an obstacle for efficient cancer therapy. Therefore, identification the kinases critical for this rewiring process in HCC is crucial.This study reveals the new role of CDK6 and its mechanistic insight in regulation of cancer stemness and drug resistance. These results support the combination treatment of lenvatinib with palbociclib for advanced HCC patients. Further studies will optimize patient target selection and identify the best treatment combinations.

2023-09-29 | PXD038152 | Pride

Clinically Relevant Proteomic Signature in Hepatocellular Carcinoma Patients with Macrovascular Invasion

Project description:Vascular invasion is considered as the critical risk factors for tumor recurrence of hepatocellular carcinoma (HCC). To reveal the molecular mechanisms underlying macrovascular invasion (MaVI) and metastasis in HCC, we performed an iTRAQ based proteomic study to identify notably dysregulated proteins in 53 HCC patients with differential vascular invasion. In patients with MaVI, 47 proteins were significantly down-regulated in HCC tumor tissue. More importantly, 30 of them were not changed in HCC without MaVI. Gene ontology analysis of these 47 proteins shows the top 3 enriched pathways are urea cycle, gluconeogenesis and arginine biosynthetic process. We validated 9 remarkably dysregulated candidates in HCC patients with MaVI by Western blot, including 8 down-regulated proteins (CPS1, ASS1, ASL, ARG1, BHMT, DMGDH, Annexin A6 and CES1) and 1 up-regulated protein (CKAP4). Furthermore, dysregulation of CPS1, ASL and ARG1, key enzymes involved in urea cycle, together with Annexin A6 and CES1, major proteins in regulating cholesterol homeostasis and fatty acid ester metabolism were verified using immunohistochemical staining. The significant down-regulation of urea cycle generates clinically relevant proteomic signature in HCC patients with macrovascular invasion, which may provide possible insights into the molecular mechanisms of metastasis and new therapeutic targets of HCC.

2022-03-02 | PXD011846 | Pride

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