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Engineered Oncolytic VSV Enhances Tumor Killing in HBV-Positive HCC

ABSTRACT: Hepatocellular carcinoma (HCC) is a leading cause of cancer-related death worldwide, with chronic hepatitis B virus (HBV) infection being a major contributor to its development. Despite this, effective treatment for HBV-associated HCC remains a significant challenge. In this study, we combined the strengths of vesicular stomatitis virus (VSV) and therapeutic vaccines to propose a novel strategy for treating HBV-related liver cancer. We engineered an oncolytic virus that delivers hepatitis B surface antigen (HBsAg) and the IL-15 cytokine directly to tumor cells, thereby enhancing immune activation and promoting tumor cell destruction. As the tumor cells die, they release additional virus particles, spreading HBsAg and IL-15 expression to neighboring tumor cells. This approach demonstrated promising efficacy in multiple HBV-positive HCC mouse models.

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

PROVIDER: MTBLS12196 | MetaboLights | 2025-07-17

REPOSITORIES: MetaboLights

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Publications

The hallmarks of cancer metabolism: Still emerging.

Pavlova Natalya N NN Zhu Jiajun J Thompson Craig B CB

Cell metabolism 20220204 3

Metabolism of cancer cells is geared toward biomass production and proliferation. Since the metabolic resources within the local tissue are finite, this can lead to nutrient depletion and accumulation of metabolic waste. To maintain growth in these conditions, cancer cells employ a variety of metabolic adaptations, the nature of which is collectively determined by the physiology of their cell of origin, the identity of transforming lesions, and the tissue in which cancer cells reside. Furthermor ...[more]

PMID: 35123658

Publication: 1/2

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Project description:Chronic infections by hepatitis B virus (HBV) and hepatitis C virus (HCV) appear to be the most significant causes of hepatocellular carcinoma (HCC). Aberrant promoter methylation is known to be deeply involved in cancer, including HCC. In this study, we analyzed aberrant promoter methylation on genome-wide scale in 6 HCCs including 3 HBV-related and 3 HCV-related HCCs, 6 matched noncancerous liver tissues and 3 normal liver tissues by methylated DNA immunoprecipitation-on-chip analysis. Candidate genes with promoter methylation were detected more frequently in HCV-related HCC. Candidate genes methylated preferentially to HBV-related or HCV-related HCCs were detected and selected, and methylation levels of the selected genes were validated using 125 liver tissue samples, including 61 HCCs (28 HBV-related HCCs and 33 HCV-related HCCs) and matched 59 matched noncancerous livers, and 5 normal livers, by quantitative methylation analysis using MALDI-TOF mass spectrometry. Among analyzed genes, preferential methylation in HBV-related HCC was validated in 1 gene only. However, 15 genes were found methylated preferentially in HCV-related HCC, which was independent from age. Hierarchical clustering of HCC using these 15 genes stratified HCV-related HCC as a cluster of frequently methylated samples. The 15 genes included genes inhibitory to cancer-related signaling such as RAS/RAF/ERK and Wnt/b-catenin pathways. It was indicated that genes methylated preferentially in HCV-related HCC exist, and it was suggested that DNA methylation might play an important role in HCV-related HCC by silencing cancer-related pathway inhibitors. we analyzed aberrant promoter methylation in 6 HCC clinical samples (including 3 HBV-related HCCs and 3 HCV-related HCCs) and their matched noncancerous tissues on genome-wide scale by the method. Candidate regions of promoter methylation preferentially to HBV-related HCC and HCV-related HCC were selected, and the methylation levels of these genes were measured quantitatively using MALDI-TOF mass spectrometry. Expression levels of these 6 pairs of HCC and 4 more pairs of HCCs and surrounding noncancerous tissues were analyzed by expression array and are reported in this Series. <br><br>This experiment was reloaded in November 2010 after additional curation. this dataset is part of the TransQST collection.

			Action	DRS
	NEG_GFP1.wiff	Wiff
	NEG_GFP1.wiff.scan	Wiff
	NEG_GFP2.wiff	Wiff
	NEG_GFP2.wiff.scan	Wiff
	NEG_GFP3.wiff	Wiff