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Barcena-Varela, M.

Publications and source records attributed to Barcena-Varela, M..

2 recordsLinked to original sources

Bacteroidetes promote hepatocellular carcinoma progression and resistance to immunotherapy

Background and AimsGrowing evidence highlight the critical role of the gut microbiome in tumorigenesis and response to immunotherapies. However, the impact of gut microbes on hepatocellular carcinoma (HCC) progression and response to immune-checkpoint blockade (ICB) remains unclear due to the lack of combined preclinical and clinical studies. Approach & ResultsWe performed 16S rRNA of cross-cohort stool samples from 10 HCC responders (R) and 40 non-responders (NR) to ICB at baseline and on-treatment time-points. We identified an enrichment of Bacteroidetes in NR. To study the role of the microbiome in the cancer immune response, we generated an immunogenic mouse model of HCC via hydrodynamic tail-vein injection (HDTVI) of DNA plasmids mimicking common HCC alterations and immunogenicity by expressing model antigens (MYC-lucOS;CTNNB1 tumors). We found that antibiotic (ABX)-induced dysbiosis promoted a pro-tumorigenic effect in the MYC-lucOS;CTNNB1 HCC model by the expansion of a specific Bacteroidetes, Parabacteroides distasonis. Colonization of mice carrying MYC-lucOS;CTNNB1 HCCs with Parabacteroides distasonis confirmed its pro-tumorigenic effect in vivo. Furthermore, we explored the effects of colonizing with microbiotas from patients and showed that microbiota from a NR donor enriched in Bacteroidetes promoted faster tumorigenesis than microbiota from a R donor with reduced Bacteroidetes. We isolated 6 Bacteroidetes species from the NR donor, cultured them, and used them as a cocktail to colonize mice; similarly, mice transplanted with this cocktail showed increased tumorigenesis and reduced survival. ConclusionsThis study identified Bacteroidetes enrichment as a potential biomarker of ICB resistance in HCC and, by using immunogenic mouse models, established that Bacteroidetes abundance influences tumor development.

cancer biology↗

NOTCH1 drives tumor plasticity and metastasis in hepatocellular carcinoma

Background & AimsLiver cancer, the third leading cause of cancer-related mortality worldwide, has two main subtypes: hepatocellular carcinoma (HCC), accounting the majority of the cases, and cholangiocarcinoma (CAA). Notch pathway primarily regulates the intrahepatic development of bile ducts, which are lined with cholangiocytes, but it can also be upregulated in 1/3 of HCCs. To better understand the role of NOTCH1 in HCC, we developed a novel mouse model driven by activated Notch1 intracellular domain (NICD1) and MYC overexpression in hepatocytes. MethodsUsing the hydrodynamic tail-vein injection method for establishing primary liver tumors, we generated a novel murine model of liver cancer harboring MYC overexpression and NOTCH1 activation. We characterized this model histopathologically as well as transcriptomically, utilizing both bulk and single cell RNA-sequencing. We also performed functional experiments using monoclonal antibodies. ResultsMYC;NICD1 tumors displayed a combined HCC-CCA phenotype with temporal plasticity. At early time-points, histology was predominantly "cholangiocellular", which then progressed to mainly "hepatocellular". The "hepatocellular" component was enriched in mesenchymal genes and gave rise to lung metastasis. Metastatic cells were enriched in the TGFB and VEGF pathways and their inhibition significantly reduced the metastatic burden. ConclusionsOur novel mouse model uncovered NOTCH1 as a driver of temporal plasticity and metastasis in HCC, the latter of which is, in part, mediated by angiogenesis and TGF{beta} pathways. Impact and ImplicationsThis study develops a novel murine model of NOTCH1-driven liver cancer, an understudied oncogene in HCC. Using this model, we show that NOTCH1 drives plasticity in HCC and metastasis to the lungs that can be therapeutically targeted through inhibition of VEGF and TGF{beta} pathways. HighlightsO_LINOTCH1 activation in combination with MYC overexpression drives combined HCC-CCA. C_LIO_LINOTCH1 activation in hepatocytes drives temporal plasticity. C_LIO_LINOTCH1 activation drives metastasis of HCC cells to the lungs, but not of CCA cells. C_LIO_LIAngiogenesis and TGF{beta} pathways mediate NOTCH1-induced lung metastasis. C_LI Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=93 SRC="FIGDIR/small/619856v2_ufig1.gif" ALT="Figure 1"> View larger version (39K): org.highwire.dtl.DTLVardef@143c866org.highwire.dtl.DTLVardef@119ddb6org.highwire.dtl.DTLVardef@12ad951org.highwire.dtl.DTLVardef@2160b8_HPS_FORMAT_FIGEXP M_FIG C_FIG

cancer biology↗