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HN1-mediated Activation of Lipogenesis Through AKT-SREBP Signaling Promotes Hepatocellular Carcinoma Cell Proliferation and Metastasis

ABSTRACT: HN1 promotes the proliferation, migration, and invasion of HCC cells, partially through activation of the Akt-HN1-SREBP signaling pathway

ORGANISM(S): Homo sapiens

PROVIDER: GSE271950 | GEO | 2026/07/05

REPOSITORIES: GEO

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HN1-mediated Activation of Lipogenesis Through AKT-SREBP Signaling Promotes Hepatocellular Carcinoma Cell Proliferation and Metastasis

Project description:HN1-mediated Activation of Lipogenesis Through AKT-SREBP Signaling Promotes Hepatocellular Carcinoma Cell Proliferation and Metastasis

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VersicanV1 promotes proliferation and metastasis of hepatocellular carcinoma through the activation of EGFR-PI3K-AKT pathway

Project description:Versican has been reported to participate in carcinogenesis in several malignant tumors. However, the accurate role of Versican in hepatocellular carcinoma (HCC) remains an enigma. Our current study reveals that VersicanV1, a predominant isoform of Versican in liver, is significantly unregulated in HCC tissues and correlates with poor prognosis. Both in vitro and in vivo experiments show that knockdown of VersicanV1 in HCC cells attenuates cancer cells malignancy. Further studies identify the positive role of VersicanV1 in aerobic glycolysis. Mechanistic investigation discovers the activation of EGFR-PI3K-AKT pathway in HCC cells expressing high VersicanV1. Moreover, EGF-like motif is indispensable for VersicanV1 to promote Warburg effect of HCC cells and subsequently, proliferation, invasion and metastasis ability via activation of EGFR-PI3K-AKT axis. Taken together, our research highlights a novel role of VersicanV1 in the progression of HCC, suggesting that VersicanV1 is an indicator for prognosis and a potential therapeutic target of HCC.

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Cdk8 attenuates lipogenesis by inhibiting SREBP-dependent transcription in Drosophila

Project description:Fine-tuning of lipogenic gene expression is important for the maintenance of long-term homeostasis of intracellular lipids. The SREBP family of transcription factors are master regulators that control the transcription of lipogenic and cholesterogenic genes, but the mechanisms modulating SREBP-dependent transcription are still not fully understood. We previously reported that CDK8, a subunit of the transcription co-factor Mediator complex, phosphorylates SREBP at a conserved threonine residue. Here, using Drosophila as a model system, we observed that the phosphodeficient SREBP proteins (SREBP-Thr390Ala) were more stable and more potent in stimulating the expression of lipogenic genes and promoting lipogenesis in vivo than wild-type SREBP. In addition, starvation blocked the effects of wild-type SREBP-induced lipogenic gene transcription, whereas phosphodeficient SREBP was resistant to this effect. Furthermore, our biochemical analyses identified six highly conserved amino acid residues in the N-terminus disordered region of SREBP that are required for its interactions with both Cdk8 and the MED15 subunit of the small Mediator complex. These results support that the concerted actions of Cdk8 and MED15 are essential for the tight regulation of SREBP-dependent transcription.

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Inhibition of GSK3 and TSC2 Mediates the Oncogenic Activity of AKT in Hepatocellular Carcinoma

Project description:Aberrant activation of AKT is a key oncogenic driver in hepatocellular carcinoma (HCC). As AKT activates multiple downstream signaling pathways, the key mechanisms mediating AKT-driven tumorigenesis must be elucidated to develop optimal treatment strategies. Using an Akt/NRas-induced HCC mouse model, we found that AKT promotes tumorigenesis by targeting TSC2 and GSK3α&β rather than FOXO family members. Loss of either TSC2, leading to mTORC1 activation, or both GSK3 isoforms cooperated with activated NRAS to promote HCC formation in vivo, albeit with different latencies. Simultaneous TSC2 and GSK3α&β deletion cooperated with NRAS to rapidly induce HCC formation, mirroring observations from the Akt/NRas HCC model. RNA-seq studies indicated distinct pathways regulated by TSC2/mTORC1 and GSK3α&β during hepatocarcinogenesis, with FOXM1 functioning as a major effector of GSK3. In summary, these findings uncover AKT’s role in suppressing the TSC complex and GSK3 to drive HCC, offering mechanistic insights into oncogenic signaling and potential therapeutic targets.

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Next Generation Sequencing Facilitates Quantitative Analysis of SREBP transgenic and SREBP/Endotrophin Transcriptomes

Project description:Purpose: The goals of this study are to compare NGS-derived liver transcriptome profiling (RNA-seq). Methods: Alb-CRE/rosa26 rtTA/SREBP(S1a/Ctrl) vs Alb-CRE/rosa26 rtTA/SREBP/TRE-ETP (S1a/ETP) transgenic mice liver (RNAseq) Results: an increase in the levels of markers that are important for immune responses and inflammation and initiating and promoting tumour growth . In addition, genes abundantly expressed in neutrophils (Elane, Mpo, Ngp, Prtn3, Chil3, Cd177, S100a8, S100a9, and Lcn-2) were up-regulated Conclusions: Our data reveal that ETP can act as a “second hit” during NAFLD progression and can play an important role in the development of NASH and hepatocellular carcinoma (HCC).

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Oncogenic activation of PI3K-AKT-mTOR signaling suppresses ferroptosis via SREBP-mediated lipogenesis.

Project description: Not available

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Activation of SREBP in Alveolar Type II Cells Enhances Lipogenesis Causing Pulmonary Lipotoxicity

Project description:Background: Lung function is dependent upon the precise regulation of the synthesis, storage, and catabolism of tissue and alveolar lipids. Results: Activation of SREBP (Sterol Response Element Binding Protein) induced lipogenesis in alveolar epithelial cells, causing neutral lipid accumulation, lung inflammation, and tissue remodeling. Conclusions: The accumulation of neutral lipids in type II epithelial cells and alveolar macrophages caused lung inflammation, consistent with findings in lipid storage disorders. Significance: Pulmonary lipotoxicity may contribute to the pathogenesis of lung dysfunction associated with diabetes, obesity, and other metabolic disorders. Genome-wide transcription profiling comparison between doxycycline-exposed SFTPC-rtTAWT/Tg/(tetO)7CMV-CreWT/Tg/Insig1flox/flox/Insig2-/- mice (i.e., Insig1/2∆/∆ ) and Insig1flox/flox/Insig2-/- . Three independent pooled RNA from isolated lung type 2 cells of each genotype were used.

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Targeting mTORC2-Dependent AKT/FOXO1/RNF125 Signaling Exploits a Therapeutic Vulnerability in c-MET-Activated and β-catenin-Mutated Hepatocellular Carcinoma

Project description:Background and Aims: Approximately 10% of human hepatocellular carcinomas (HCC) exhibit concurrent c-MET activation and β-catenin gain-of-function mutations, representing a clinically relevant HCC subtype. This study aimed to investigate the role of mTORC2/AKT signaling in this subtype and identify potential therapeutic targets. Approach and Results: The mTORC2/AKT cascade was activated in c-Met/β-cateninΔ90 HCC lesions. Genetic ablation of Rictor, the essential mTORC2 subunit, strongly suppressed c-Met/β-cateninΔ90-dependent hepatocarcinogenesis. Mechanistically, both the TSC2/mTORC1 axis and FOXO1 transcription factors functioned as critical downstream effectors of mTORC2/AKT in this model. We further identified RNF125 as a direct transcriptional target of FOXO1. RNF125 overexpression significantly inhibited tumorigenesis in the c-Met/β-cateninΔ90 model and suppressed liver cancer cell growth in vitro. Notably, using an in vivo doxycycline-inducible system, we found that inducing RNF125 expression in established c-Met/β-cateninΔ90 HCC suppressed tumor progression, suggesting that activation of RNF125 may have translational implications for HCC treatment. Conclusions: Our study, for the first time, established the mTORC2/AKT/FOXO1/RNF125 axis as a critical driver and therapeutic vulnerability in c-MET-activated/β-catenin-mutated HCC. Our study filled a critical gap by defining the tumor-suppressive role of FOXO1 specifically in this HCC subtype. Furthermore, our results positioned RNF125 as a promising therapeutic target for this aggressive HCC subtype.

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Activation of SREBP in Alveolar Type II Cells Enhances Lipogenesis Causing Pulmonary Lipotoxicity

2012-03-01 | GSE31797 | GEO