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The role and mechanism of hypoxia-induced SLC6A8 up-regulation in HCC progression

ABSTRACT: The role and mechanism of hypoxia-induced SLC6A8 up-regulation in HCC progression

PROVIDER: PRJNA1224831 | ENA |

REPOSITORIES: ENA

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The role and mechanism of hypoxia-induced SLC6A8 up-regulation in HCC progression

Project description:Hypoxia is a hallmark of solid tumors and profoundly affects the malignant phenotypes of cancer cells. We find that the creatine transporter solute carrier family 6, member 8 (SLC6A8) is upregulated in hypoxic HCC cells. Hypoxia-induced creatine accumulation drives metabolic reprogramming and antagonizes parthanatos. Pharmacological inhibition of SLC6A8 represents a promising therapeutic strategy for HCC.

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Chronic intermittent hypoxia in DEN-induced rat model of HCC

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Hypoxia-induced CD147-enriched migrasomes promote sorafenib resistance in HCC by inducing vasculogenic mimicry via PI3K/AKT/TWIST1 signaling

Project description:Conventional anti-angiogenic drugs (AADs) combined with sorafenib have little success in HCC patients, as the formation of hypoxia areas in tumors and vasculogenic mimicry’s (VM's) non-responsiveness to AADs. Migrasomes are recently discovered extracellular vesicles produced during cell migration. In this study, the results show that hypoxia-induced migrasomes induce the formation of VM and promote the sorafenib resistance. Further studies reveal that hypoxia-induced migrasomes can be taken up by HCC cells via macropinocytosis, which activates PI3K/AKT/TWIST1 signaling. Moreover, CD147 on the surface of hypoxia-induced migrasomes is identified as a key protein in regulating the signaling pathway. Overall, our findings uncover a previously unrecognized mechanism mediated by hypoxia-induced migrasomes and the formation of VM and provide a new method for preventing SFR.

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Project description:Hepatocellular carcinoma (HCC) is a formidable malignancy with limited effective therapeutic avenues. This study was designed to investigate the role of transglutaminase 2 (TGM2) in promoting HCC progression and assess its potential as a target for therapeutic intervention in HCC treatment.TMG2 expression was positively related to a higher AFP level, poor differentiation, and a later BCLC stage. Tgm2 deficiency or H3Q5ser inhibition notably restrained HCC progression. Mechanism research revealed that TGM2-mediated H3Q5ser modifications promote HCC progression via MYC pathway signaling. Furthermore, transcriptional intermediary factor 1 beta (TIF1-β/TRIM28) mediated the recruitment of TGM2 by MYC to facilitate H3Q5ser modifications on MYC targets. Finally, targeting the TGM2 transglutaminase activity significantly suppressed HCC progression in preclinical models.

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The role and mechanism of hypoxia in regulating parthanatos in hepatocellular carcinoma

Project description:Recently, a PARP1-dependent cell-death process termed "parthanatos", driven by DNA damage, has emerged as a crucial regulator of tissue homeostasis and tumorigenesis. Hypoxia is a hallmark of solid tumors and profoundly affects the malignant phenotypes of cancer cells. The crosstalk between parthanatos and hypoxia remains poorly understood. In our study, we find that despite causing DNA damage, hypoxia fails to induce parthanatos in HCC. Transcriptome sequencing upon MNNG stimulation indicated that the creatine transporter solute carrier family 6, member 8 (SLC6A8) was involved in parthanatos antagonism and malignant phenotypes in hypoxic HCC cells.

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Effect of hypoxia on gene expression in Hep3B cells

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Project description:Introduction: The progression of hepatocellular carcinoma (HCC) is intricately linked to complex interactions within the tumor microenvironment (TME), where the reprogramming of tumor-associated macrophages (TAMs) plays a pivotal role. However, how HCC cells regulate TAM metabolism and function via extracellular vesicles, such as exosomes, remains incompletely understood. Methods: We isolated exosomes from HCC cell lines and co-cultured them with macrophages. Using proteomics, lipid analysis, flow cytometry, and animal models, we evaluated the effects of exosomal FABP5 on macrophage polarization and lipid metabolism. The role of FABP5 in tumor progression was assessed via in vivo experiments. Results: This study reveals that HCC cells release fatty acid-binding protein 5 (FABP5) via exosomes, transferring it to TAMs, thereby inducing significant lipid metabolism reprogramming in macrophages. Mechanistically, exosomal FABP5 promotes lipid accumulation by activating the PPARγ signaling pathway, while potentially inhibiting the PPARα signaling pathway to reduce fatty acid oxidation, ultimately driving TAM polarization towards an M2 phenotype, characterized by increased secretion of immunosuppressive cytokines and a pro-tumor phenotype. Clinical data analysis indicates that high FABP5 expression in HCC tissues correlates with poor patient prognosis. In liver-specific FABP5 knockout mouse models and HCC xenograft models, FABP5 deletion significantly suppressed tumor growth, reduced M2-type TAM infiltration and lipid accumulation, and enhanced anti-tumor immune responses. Conclusion: These findings collectively uncover exosomal FABP5 as a key mediator of metabolic and immune communication between HCC and TAMs, promoting HCC progression by remodeling the tumor immune microenvironment, and suggest FABP5 as a potential therapeutic target for HCC.

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