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Comprehensive proteometics identifies FBXL6 substrates involved in liver cancer

ABSTRACT: FBXL6 is frequently over-expressed in human hepatocellular carcinoma (HCC). However, it is still unknown the underlying mechanisms by which FBXL6 promotes HCC. In this study, we compared ubiquitinated protein profiles among a panel of liver tissue samples (including HCC, adjacent tissues and normal tissues) from Fbxl6LSL-fl/+; Alb-cre mice and Alb-cre mice by proteomics and ubiquitomics analysis. There are many proteins with ubiquitination in FBXL6 overexpressed HCC, suggesting ubiquitination may play a critical role in FBXL6-mediated HCC. A1--- normal tissue 1 A2--- normal tissue 2 B1--- Adjacent tissue 1 B2--- Adjacent tissue 2 C1--- HCC tissue 1 C2--- HCC tissue 2

INSTRUMENT(S): Orbitrap Fusion

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Liver

SUBMITTER: Chuanming Xie

LAB HEAD: Chuanming Xie

PROVIDER: PXD032357 | Pride | 2024-01-26

REPOSITORIES: Pride

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	B.zip	Other
	C.zip	Other
	S9093LPUb_A1.raw	Raw
	S9093LPUb_A2.raw	Raw

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Publications

Elevated FBXL6 expression in hepatocytes activates VRK2-transketolase-ROS-mTOR-mediated immune evasion and liver cancer metastasis in mice.

Zhang Jie J Lin Xiao-Tong XT Yu Hong-Qiang HQ Fang Lei L Wu Di D Luo Yuan-Deng YD Zhang Yu-Jun YJ Xie Chuan-Ming CM

Experimental & molecular medicine 20230901 10

Metastatic hepatocellular carcinoma (HCC) is the most lethal malignancy and lacks effective treatment. FBXL6 is overexpressed in human hepatocellular carcinoma (HCC), but whether this change drives liver tumorigenesis and lung metastasis in vivo remains unknown. In this study, we aimed to identify FBXL6 (F-Box and Leucine Rich Repeat Protein 6) as a key driver of HCC metastasis and to provide a new paradigm for HCC therapy. We found that elevated FBXL6 expression in hepatocytes drove HCC lung me ...[more]

PMID: 37653031

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The potential biomarkers for HCC patients with functional loss of both p53 and Tsc1

Project description:p53 mutations occur frequently in human hepatocellular carcinoma (HCC). Activation of the mammalian target of rapamycin (mTOR) pathway is also associated with HCC. However, it is still unknown whether these changes together initiate HCC and can be targeted as a potential therapeutic strategy. Here, we compared transcriptional profiles among a panel of liver tissue samples from p53+/-, Tsc1fl/fl;Alb-cre, and p53+/-;Tsc1fl/fl;Alb-cre mice by RNAseq analysis. The overlapping genes in those three genotypes were considered potential biomarkers for HCC patients with functional loss of both p53 and Tsc1.

2021-08-30 | GSE153223 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of three groups from mouse liver Transcriptomes

Project description:Liver mRNA profiles of WT liver(WT1-WT3) and Alb-Cre:Hdac3−/− liver (0d(Ha-Hc), 7d(Hd-Hg), 21d(Hh-Hk), 50d(Hl-Hn)) receiving successive PH(sPH), Alb-Cre:Hdac3−/− tumor tissues(HCC1-HCC3) and adjacent non-tumor tissues(N1-N3), spontaneous liver cancers of Alb-Cre:Hdac3-/- mice (HCC1-HCC3) and liver tumor of recipient Fah-/- mice (HCCa-HCCc) were generated by deep sequencing.

2021-05-11 | GSE114503 | GEO

Differential proteomics between AFP-negative HCC and adjacent non-tumor liver tissue

Project description:We screened and identified novel proteins in AFP-negative HCC tissue that were differentially expressed related to levels in adjacent non-tumor liver tissue using SWATH-MS proteome technology

2021-11-02 | PXD028854 | Pride

HAF prevents hepatocyte apoptosis and progression to MASH and hepatocellular carcinoma through transcriptional regulation of the NF-kB pathway

Project description:Background: HCC incidence is increasing worldwide due to the obesity epidemic, which drives metabolic dysfunction-associated steatohepatitis (MASH) that can lead to HCC. However, the molecular pathways driving MASH-HCC are poorly understood. We have previously reported that male mice with haploinsufficiency of hypoxia-associated factor, HAF (SART1+/-) spontaneously develop MASH-HCC. However, the cell type(s) responsible for HCC associated with HAF loss are unclear. Results: We generated SART1-floxed mice, which were crossed with mice expressing Cre-recombinase within hepatocytes (Alb-Cre; hepS-/-) or myeloid cells (LysM-Cre, macS-/-). HepS-/- mice (both male and female) developed HCC associated with profound inflammatory and lipid dysregulation suggesting that HAF protects against HCC primarily within hepatocytes. HAF-deficient hepatocytes showed decreased P-p65 and P-p50 and in many components of the NF-kB pathway, which was recapitulated using HAF siRNA in vitro. HAF depletion also triggered apoptosis, suggesting that HAF protects against HCC by suppressing hepatocyte apoptosis. We show that HAF regulates NF-kB activity by regulating transcription of TRADD and RIPK1. Mice fed a high-fat diet (HFD) showed marked suppression of HAF, P-p65 and TRADD within their livers after 26 weeks, but showed profound upregulation of these proteins after 40 weeks, implicating deregulation of the HAF-NF-kB axis in the progression to MASH. In humans, HAF was significantly decreased in livers with simple steatosis but significantly increased in HCC compared with normal liver. Conclusions: HAF is novel transcriptional regulator of the NF-kB pathway and is a key determinant of cell fate during progression to MASH and MASH-HCC.

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Expression data from AEG-1fl/fl and AEG-1DHEP mice which have conditional hepatocyte-specific knockout of AEG-1 (Astrocyte elevated gene 1)

Project description:AEG-1 is overexpressed in human hepatocellular carcinoma (HCC) and positively regulates development and progression of HCC A conditional hepatocyte-specific knockout mouse was generated by crossing floxed AEG-1 mouse with Alb/Cre mouse in C57BL/6 background

2017-08-02 | GSE85098 | GEO

Murine hepatocellular carcinoma of MCL1-/- transgenic mice and age matched alb cre mice - 12 months old.

2009-12-31 | GSE16580 | GEO

Small RNA Solexa sequencing of human liver samples

Project description:We applied small RNA Solexa sequencing technology to identify microRNA expression in human liver samples from surgically removed liver tissues including three normal liver tissues (distal normal liver tissue of liver hemangioma), an hepatitis B virus (HBV)-infected liver, a severe chronic hepatitis B liver, two HBV-related hepatocellular carcinoma (HCC), an hepatitis C virus (HCV)-related HCC, and an HCC without HBV or HCV infection. All samples were collected with the informed consent of the patients and the experiments were approved by the ethics committee of Second Military Medical University, Shanghai, China. We investigated the miRNome in human normal liver and suggested some deregulated abundantly expressed microRNAs in HCC. center_name: National Key Laboratory of Medical Immunology & Institute of Immunology, Second Military Medical University, Shanghai, China. Examination of miRNome in human liver samples from surgically removed liver tissues including three normal liver tissues (distal normal liver tissue of liver hemangioma), an hepatitis B virus (HBV)-infected liver tissue, a severe chronic hepatitis B liver tissue, an HBV-related hepatocellular carcinoma (HCC) tissue and adjacent liver tissues of different regions,an HBV-related HCC tissue and adjacent liver tissue, an hepatitis C virus (HCV)-related HCC tissue and adjacent liver tissue, and an HCC without HBV or HCV infection and adjacent liver tissue. All 15 human liver tissue samples.

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Comparative analysis of proteomics between lymphocyte-rich hepatocellular carcinoma and hepatocellular carcinoma formalin fixed and paraffin embedded tissues

Project description:In this study, the proteomic tissue proteins were analyzed using LC-MS. Fifteen lymphocyte-rich HCC formalin fixed and paraffin embedded (FFPE) tissues, 15 adjacent normal FFPE tissues, and 15 HCC FFPE tissues were analyzed. More than 4,000 liver tissue proteins have been identified by high-sensitivity nanoflow liquid chromatography-tandem mass spectrometry (LC-MS/MS).

2024-02-21 | PXD037022 | Pride

Murine hepatocellular carcinoma of MCL1-/- transgenic mice and age matched alb cre mice - 12 months old.

Project description:aCGH analysis of murine transgenic liver tissues affected with HCC, hybridized with age (12 months) and sex matched alb cre mice. Keywords: Array comparative genomic hybridization analysis (aCGH). Independent HCC of MCL1-/- mice were hybridized with pooled wt mice. Mclâ1flox/flox mice (C57BL/6 background) were obtained from the Dana Farber Cancer Institute, Boston, USA (Opferman JT et al., Nature 2003) and bred to heterozygous Albumin-Cre mice (C57BL/6 background) which led to hepatocyte-specific deletion of Mcl-1. The mice develop severe chronic liver damage (Vick B et al., Hepatology, 2009).

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Expression data from WT SIRT6 and SIRT6 albumin CRE conditional mice

Project description:Microarray analysis of liver tissue from WT SIRT6 and conditional knockout of SIRT6 using albumin-Cre (SIRT6Co/Co ;Alb-Cre) at 2 and 8 months of age RNA was extracted from mouse liver tissue at 2 and 8 months of age. RNA from three pairs of WT SIRT6 and SIRT6Co/Co ;Alb-Cre mice was combined and hybridized to Affymetrix mouse gene 1.0 ST arrays.

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