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ABSTRACT: Lenvatinib-resistant HCC cell RNA-seq

PROVIDER: PRJNA1130017 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29655372_1.fastq.gz	Fastqsanger.gz
	SRR29655372_2.fastq.gz	Fastqsanger.gz
	SRR29655373_1.fastq.gz	Fastqsanger.gz
	SRR29655373_2.fastq.gz	Fastqsanger.gz
	SRR29655374_1.fastq.gz	Fastqsanger.gz

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Project description:Lenvatinib-resistant HCC cell RNA-seq

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GOLM1 dictates acquired Lenvatinib resistance by a GOLM1-CSN5 positive feedback loop upon EGFR signaling activation in hepatocellular carcinoma

Project description:Lenvatinib is a multiple receptor tyrosine kinases inhibitor (TKI) authorized for first-line treatment of hepatocellular carcinoma (HCC). However, Lenvatinib resistance is common in HCC clinical treatment, highlighting the urgent need to understand mechanisms of resistance. Here, we identified Golgi membrane protein 1 (GOLM1), a type II transmembrane protein originally located in the Golgi apparatus, as a novel regulator of Lenvatinib resistance. We established Lenvatinib resistance in human HCC cell lines PLC/PRF/5. Through RNA-seq, we found that GOLM1 was significantly upregulated, which was further validated in patients derived tumor tissue and peripheral blood. GOLM1 overexpression contributes to Lenvatinib resistance and HCC progression in vitro and in vivo. Mechanistically, GOLM1 upregulates CSN5 expression through EGFR-STAT3 pathway. Reversely, CSN5 deubiquitinates and stabilizes GOLM1 protein by inhibiting ubiquitin-proteasome pathway of GOLM1. Collectively, our data demonstrate that GOLM1 is one of the key driver of Lenvatinib resistance in HCC and depicts a molecular network in Lenvatininb resistant HCC cells.

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Establishment and Characterization of Mouse Metabolic dysfunction-associated steatohepatitis-related Hepatocellular carcinoma organoids

Project description:Metabolic dysfunction-associated steatohepatitis is a form of chronic liver inflammation associated with metabolic syndrome, such as obesity and a major cause of hepatocellular carcinoma. Multi-biotics, a soymilk fermented with lactic acid bacteria, are known to alleviate obesity by lowering lipid profile. In this study, we investigated efficacy of multi-biotics in MASH-related HCC using mouse model fed choline-deficient L-amino acid-defined high-fat diet, and determined that tumor regression was not affected by multi-biotics. We established mouse MASH-related HCC organoids, and performed RNA-sequencing to identify transcriptomic features in MASH-HCC treated multi-biotics. We also examined response of MASH-related HCC to four HCC treatment drugs, and MASH-related HCC treated multi-biotics was good response to Lenvatinib. We established Lenvatinib-resistant MASH-related HCC organoids by administrating repeatedly Lenvatinib, and identified enriched pathways in Lenvatinib-resistant models. This study provides a tool for studying MASH-related HCC treatment and Lenvatinib resistance by establishing the MASH-related HCC and Lenvatinib resistance organoid model.

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RNA-seq data for parental and lenvatinib-resistant HCC cells

Project description:RNA-seq data for parental and lenvatinib-resistant HCC cells

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RNA Sequencing of HCC cells after lenvatinib, gefitinib, and combination treatment

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