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Metabolic Reprogramming in Tumor-Associated Macrophages during Murine Hepatocellular Carcinoma Progression

ABSTRACT:

To investigate the impact of Wdr4 on the metabolic reprogramming of tumor-associated macrophages (TAMs) in hepatocellular carcinoma (HCC), we established an orthotopic HCC model in Wdr4-f/f and Wdr4 conditional knockout (Wdr4-cKO) mice. TAMs were subsequently isolated via flow cytometry-based cell sorting. Untargeted metabolomics analysis was performed to identify metabolic alterations in TAMs associated with Wdr4 deficiency.

INSTRUMENT(S): Liquid Chromatography MS - positive, Liquid Chromatography MS - negative

PROVIDER: MTBLS12764 | MetaboLights | 2025-09-28

REPOSITORIES: MetaboLights

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			Action	DRS
	KO-1.wiff	Wiff
	KO-1.wiff.scan	Wiff
	KO-2.wiff	Wiff
	KO-2.wiff.scan	Wiff
	KO-3.wiff	Wiff

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Publications

METTL5 stabilizes c-Myc by facilitating USP5 translation to reprogram glucose metabolism and promote hepatocellular carcinoma progression.

Xia Peng P Zhang Hao H Lu Haofeng H Xu Kequan K Jiang Xiang X Jiang Yuke Y Gongye Xiangdong X Chen Zhang Z Liu Jie J Chen Xi X Ma Weijie W Zhang Zhonglin Z Yuan Yufeng Y

Cancer communications (London, England) 20230105 3

<h4>Background</h4>Hepatocellular carcinoma (HCC) is one of the most prevalent cancers in the world, with a high likelihood of metastasis and a dismal prognosis. The reprogramming of glucose metabolism is critical in the development of HCC. The Warburg effect has recently been confirmed to occur in a variety of cancers, including HCC. However, little is known about the molecular biological mechanisms underlying the Warburg effect in HCC cells. In this study, we sought to better understand how me ...[more]

PMID: 36602428

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RNA-seq for tumor associated macrophages in hepatocellular carcinoma

Project description:To investigate the relationship between MIF and SPP1, we induced THP-1 cells with lentivirus carrying SPP1 shRNA and negative control virus into HCC-TAMs and 4IPP-treated HCC-TAMs (tumor associated macrophages in hepatocellular carcinoma).

2023-07-10 | GSE230666 | GEO

A tumor endothelial cell-specific microRNA replacement therapy for hepatocellular carcinoma

Project description:Current approved anti-angiogenic drugs (AAD) for hepatocellular carcinoma (HCC) inhibit tumor angiogenesis, but affect the hepatic vasculature resulting in adverse effects. Tumor endothelial cells (TECs) differ from normal endothelial cells. In this study, we aimed to detect TEC-specific miRNAs and develop an anti-angiogenic treatment specific for TECs. We established HCC orthotopic mouse models. TEC-specific miRNAs were detected using a microRNA array. Finally, we evaluated the therapeutic effects of the TEC-specific miRNA agonist cocktail. In total, 260 TEC-specific genes were detected. Among the top ten downregulated TEC-specific miRNAs, miR-139-3p and 214-3p were important for the TEC phenotype. The TEC-specific microRNA agonist cocktail showed significant anti-tumor effects by inhibiting tumor angiogenesis without affecting hepatic vasculatures in HCC orthotopic mouse models. Moreover, it significantly downregulated tip-cell sprouting-related genes. We identified two downregulated TEC-specific miRNAs; microRNA replacement therapy, which targets the downregulated TEC-specific miRNAs, is an effective and promising treatment for HCC

2024-02-07 | GSE250147 | GEO

3-D culture cell lines mimic tumor in hepatocellular carcinoma

Project description:Hepatocellular carcinoma (HCC) is one of the main subtypes of primary liver cancer, which accounts for 75-85% of all cases [1]. Despite increasing availability of treatments for liver cancer, HCC clinical trials are not promising since most HCC patients are in an advanced stage of HCC at the time of diagnosis. Additionally, highly metastatic and recurrent phenotype aggravate poor prognosis of liver cancer [2]. Therefore, there is an urgent need to explore the underlying molecular mechanism in HCC progression.

2023-09-18 | PXD036831 | JPOST Repository

Proteomic characterization of human hepatocellular carcinoma (HCC) tumor biopsies

Project description:We analyzed the proteome of tumor and matched non-tumor biopsies from 51 treatment-naive Hepatocellular carcinoma (HCC) patients by DIA (SWATH). Thereby we aim to find subgroups of patients characterized by specific pathway activation. Furthermore, we aim to find novel factors involved in HCC development and novel biomarkers.

2022-03-14 | PXD025705 | Pride

Phospho-proteomic characterization of human hepatocellular carcinoma (HCC) tumor biopsies

Project description:We analyzed the phospho-proteome of tumor and matched non-tumor biopsies from 51 treatment-naive Hepatocellular carcinoma (HCC) patients by label-free DDA. Thereby we aim to find subgroups of patients characterized by specific pathway activation. Furthermore, we aim to find novel factors involved in HCC development and novel biomarkers.

2022-03-14 | PXD025836 | Pride

Fasting reverses drug-resistance in hepatocellular carcinoma through p53-dependent metabolic synergism

Project description:Cancer cells voraciously consume nutrients to support their growth, exposing a metabolic vulnerability that can be therapeutically exploited. Here we show in hepatocellular carcinoma (HCC) cells, xenografts, and in patient-derived HCC organoids that fasting can synergistically sensitise resistant HCC to sorafenib. Mechanistically, sorafenib acts non-canonically as inhibitor of mitochondrial respiration, causing resistant cells to depend on glycolysis for survival. Fasting, through reduction in glucose and impeded AKT/mTOR-signalling, prevents this Warburg shift. p53 is necessary and sufficient for the sorafenib-sensitizing effect of nutrient restriction and crucial for improvement of sorafenib efficacy through intermittent fasting (IF) in an orthotopic HCC mouse model. Together, our data indicate IF and sorafenib as clinically actionable, rational combination therapy for HCC with intact p53 signalling. As HCC therapy is currently severely limited by resistance, these results should instigate clinical studies with the goal of improving therapy response in advanced-stage, and possibly even early-stage, HCC.

2022-02-16 | PXD022723 | Pride

Spermine Synthase Engages in Macrophages M2 polarization to Sabotage Antitumor Immunity in Hepatocellular Carcinoma

Project description:Disturbances in tumor cell metabolism reshape the tumor microenvironment (TME) and impair antitumor immunity, but the implicit mechanisms remain elusive. Here, we found that spermine synthase (SMS) was significantly upregulated in tumor cells, which correlated positively with immunosuppressive microenvironments and predicted poor survival in hepatocellular carcinoma (HCC) patients. Via “subcutaneous” and “orthotopic” HCC syngeneic mouse models and a series of in vitro coculture experiments, we identified elevated SMS level in HCC cells played a role in immune escape mainly through its metabolic product spermine, which induced tumor-associated macrophage (TAM) reprogramming and subsequently corresponded with a decreased antitumor functionality of CD8+ T cells. Mechanistically, we discovered that spermine reprogrammed TAM mainly by activating the PI3K-Akt-mTOR-S6K signaling pathway. Spermine inhibition in combination with immune checkpoint blockade effectively diminishes tumor burden in vivo. Our results expand the understanding of the critical role of metabolites in regulating cancer progression and anti-tumor immunity, and open new avenues for developing novel therapeutic strategies against HCC.

2024-11-11 | GSE277457 | GEO

Copy number alterations of 103 hepatocellular carcinomas with hepatitis C virus etiology

Project description:To characterize the genetic alterations that instigate hepatitis C virus-induced hepatocellular carcinoma (HCC), we conducted an integrative genomic analysis of 103 HCCs. Most tumors harbored 1q gain, 8q gain or 8p loss, with occasional alterations in 13 additional chromosome arms. In addition to amplifications at 11q13 in 6 tumors, 4 tumors harbored focal gains at 6p21 incorporating VEGFA, which were confirmed in 4 of 113 HCC in an independent validation set. Strikingly, this locus overlapped with copy gains in 4 of 371 lung adenocarcinomas. Overexpression of VEGFA via 6p21 gain suggested a cell-nonautonomous mechanism of oncogene activation. Hierarchical clustering of gene expression among 91 tumors identified 5 classes, including ‘Wnt-CTNNB1’, ‘proliferation’ and ‘interferon-related’ gene classes. We also discovered a novel class defined by polysomy of chromosome 7, gains of which were associated with early tumor recurrence after resection. These findings reveal key alterations in HCC pathogenesis and implicate potential therapeutic targets. Keywords: disease state analysis 103 hepatocellular carcinomas and 95 adjacent cirrhotic, non-tumoral liver tissue were obtained at the time of surgical resection of orthotopic transplantation.

2008-06-21 | E-GEOD-9845 | biostudies-arrayexpress

Transcription profiling by array of human hepatocellular carcinomas with hepatitis C virus etiology

Project description:To characterize the genetic alterations that instigate hepatitis C virus-induced hepatocellular carcinoma (HCC), we conducted an integrative genomic analysis of 103 HCCs. Most tumors harbored 1q gain, 8q gain or 8p loss, with occasional alterations in 13 additional chromosome arms. In addition to amplifications at 11q13 in 6 tumors, 4 tumors harbored focal gains at 6p21 incorporating VEGFA, which were confirmed in 4 of 113 HCC in an independent validation set. Strikingly, this locus overlapped with copy gains in 4 of 371 lung adenocarcinomas. Overexpression of VEGFA via 6p21 gain suggested a cell-nonautonomous mechanism of oncogene activation. Hierarchical clustering of gene expression among 91 tumors identified 5 classes, including 'Wnt-CTNNB1', 'proliferation' and 'nterferon-related' gene classes. We also discovered a novel class defined by polysomy of chromosome 7, gains of which were associated with early tumor recurrence after resection. These findings reveal key alterations in HCC pathogenesis and implicate potential therapeutic targets. Experiment Overall Design: 91 hepatocellular carcinomas were obtained at the time of surgical resection or orthotopic transplantation.

2008-10-25 | E-GEOD-9843 | biostudies-arrayexpress

Berberine protects against hepatocellular carcinoma progression by regulating intrahepatic T cell heterogeneity

Project description:Accumulating evidence suggests that berberine (BBR) exhibits anti-cancer effects in hepatocellular carcinoma (HCC). However, the mechanisms by which BBR regulates the immunological microenvironment in HCC has not been fully elucidated. In this study, we established a mouse model of orthotopic HCC and treated with varying doses of BBR. BBR showed effectiveness in reducing tumor burden in mice with HCC. Cytometry by time-of-flight depicted the alterations in the tumor immune landscape following BBR treatment, revealing the enhancement in the T lymphocytes effector function. In particular, BBR decreased the proportion of TCRbhiPD-1hiCD69+CD27+CD8a+ effector CD8+ T lymphocytes and increased the proportion of Ly6ChiTCRb+CD69+CD27+CD62L+ central memory CD8+ T lymphocytes. Single-cell RNA sequencing further elucidate the effects of BBR on transcriptional profiles of liver immune cell and confirmed the phenotypical heterogeneity of T lymphocytes in HCC immune microenvironment. Additionally, we found that BBR potentially regulated the antitumor immunity in HCC by modulating the receptor-ligand interaction among immune cells mediated by cytokines. In summary, our findings improve the understanding of BBR's impact on protecting against HCC, emphasizing BBR's role in regulating intrahepatic T cell heterogeneity. BBR has the potential to be a promising therapeutic strategy to hinder the advancement of HCC.

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