Lipid Metabolism in Development and Progression of Hepatocellular Carcinoma

Sangineto, Moris; Villani, Rosanna; Cavallone, Francesco; Romano, Antonino Davide; Loizzi, Domenico; Serviddio, Gaetano

doi:10.3390/cancers12061419

Cited by 114 publications

(92 citation statements)

References 186 publications

(235 reference statements)

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“…54 More recently, it has been reported that upregulation of AMPK activity, a typical nutrient deficiency condition, promoted the expressions of CPT-1 and CPT-2 and finally initiated the β-oxidation in HCC. 55 Hence, we observed the change of AMPK activation after LRP1B knockdown in HCC cells and found the upregulated activation of AMPK signaling. Herein, it…”

mentioning

confidence: 77%

<p>Effects of LRP1B Regulated by HSF1 on Lipid Metabolism in Hepatocellular Carcinoma</p>

Li¹,

Hu²,

Jin³

et al. 2020

JHC

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mentioning

confidence: 77%

<p>Effects of LRP1B Regulated by HSF1 on Lipid Metabolism in Hepatocellular Carcinoma</p>

Li¹,

Hu²,

Jin³

et al. 2020

JHC

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“…Although the Warburg effect and glutamine metabolism alterations are common processes in the metabolic reprogramming of tumors [ 21 , 22 ]. Mounting evidence also suggests that lipid metabolic reprogramming is essential for HCC development [ 23 ]. For instance, HCC cells typically exhibit enhanced de novo synthesis of fatty acids [ 24 ].…”

Section: Discussionmentioning

confidence: 99%

Development of a novel lipid metabolism-based risk score model in hepatocellular carcinoma patients

Wang

Zhang

et al. 2021

BMC Gastroenterol

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Background Liver cancer is one of the most common malignancies worldwide. HCC (hepatocellular carcinoma) is the predominant pathological type of liver cancer, accounting for approximately 75–85 % of all liver cancers. Lipid metabolic reprogramming has emerged as an important feature of HCC. However, the influence of lipid metabolism-related gene expression in HCC patient prognosis remains unknown. In this study, we performed a comprehensive analysis of HCC gene expression data from TCGA (The Cancer Genome Atlas) to acquire further insight into the role of lipid metabolism-related genes in HCC patient prognosis. Methods We analyzed the mRNA expression profiles of 424 HCC patients from the TCGA database. GSEA(Gene Set Enrichment Analysis) was performed to identify lipid metabolism-related gene sets associated with HCC. We performed univariate Cox regression and LASSO(least absolute shrinkage and selection operator) regression analyses to identify genes with prognostic value and develop a prognostic model, which was tested in a validation cohort. We performed Kaplan-Meier survival and ROC (receiver operating characteristic) analyses to evaluate the performance of the model. Results We identified three lipid metabolism-related genes (ME1, MED10, MED22) with prognostic value in HCC and used them to calculate a risk score for each HCC patient. High-risk HCC patients exhibited a significantly lower survival rate than low-risk patients. Multivariate Cox regression analysis revealed that the 3-gene signature was an independent prognostic factor in HCC. Furthermore, the signature provided a highly accurate prediction of HCC patient prognosis. Conclusions We identified three lipid-metabolism-related genes that are upregulated in HCC tissues and established a 3-gene signature-based risk model that can accurately predict HCC patient prognosis. Our findings support the strong links between lipid metabolism and HCC and may facilitate the development of new metabolism-targeted treatment approaches for HCC.

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“…The most important risk factors for HCC are HBV and HCV, the alcohol consumption and exposition to aflatoxin B1 [12,21]. The HBV or HCV related HCC are caused by chronical viral infection; whereas, the etiology of NBNC-HCC is mostly a metabolic dysregulation [27]. The tumor physiological features are quite different.…”

Section: Discussionmentioning

confidence: 99%

Fidgetin as a potential prognostic biomarker for hepatocellular carcinoma

Zhou¹,

Wang²,

Gao³

et al. 2020

Int. J. Med. Sci.

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Background: Fidgetin (FIGN), a conserved ATP-dependent enzyme, is regarded as a hepatocellular carcinoma (HCC) risk gene, but the prognostic implication of FIGN in HCC remains obscure. In this study, we investigate the expression of FIGN in HCC and to evaluate its prognostic value. Methods: A total of 216 patients with HCC who experienced hepatectomy were recruited in this study. The expression of FIGN in HCC samples was evaluated by quantitative real-time PCR, immunohistochemistry and immunoblotting analysis. And Cox regression model was used to evaluate the prognostic value of all covariates. Results: Of the 216 HCC patients, 67 (31.0%) had tumors with high FIGN expression and 149 (69.0%) had tumors with low FIGN expression. FIGN expression was positively correlated with TNM stage (P = 0.039), tumor with incomplete capsule (P = 0.036), microvascular invasion (P = 0.023), and portal vein tumor thrombus (P = 0.003). High expression of FIGN indicated shorter overall survival (OS) (hazard ratio: 4.569, P = 0.036) and disease-free survival (DFS) (hazard ratio: 6.487, P = 0.001). Conclusion: Our results indicate that high Fidgetin expression is associated with tumor progression and suggest a worse prognosis in HCC. Fidgetin might serve as a potential target for therapy.

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Lipid Metabolism in Development and Progression of Hepatocellular Carcinoma

Cited by 114 publications

References 186 publications

<p>Effects of LRP1B Regulated by HSF1 on Lipid Metabolism in Hepatocellular Carcinoma</p>

<p>Effects of LRP1B Regulated by HSF1 on Lipid Metabolism in Hepatocellular Carcinoma</p>

Development of a novel lipid metabolism-based risk score model in hepatocellular carcinoma patients

Fidgetin as a potential prognostic biomarker for hepatocellular carcinoma

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