Global miRNA sequencing upon HDAC inhibition in HCC
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA756298 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15529900.fastq.gz | Fastqsanger.gz | |||
| SRR15529901.fastq.gz | Fastqsanger.gz | |||
| SRR15529902.fastq.gz | Fastqsanger.gz | |||
| SRR15529903.fastq.gz | Fastqsanger.gz | |||
| SRR15529904.fastq.gz | Fastqsanger.gz |
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Project description:To find potential target gene of ZNF281 in HCC cells, the transcriptome analyse (RNA-seq) were performed in HLE HCC cell lines with or with ZNF281 depletion using shRNAs in lentivirus vectors Zinc finger protein 281 (ZNF281) has been implicated in the progression of several types of cancer. However, its functionality and transcriptional targets in hepatocellular carcinoma (HCC) remains elusive. In the present study, we discovered that the expression of ZNF281 was increased in tumor tissues and cell lines, and positively correlated with vessel invasion in HCC. We took RNA interference approach and constructed 2 shRNAs lentivirus vectors targeting different regions of ZNF281 which were named as ZNF281.kd1 and ZNF281.kd2 respectively. Knockdown of ZNF281 suppressed proliferation, migration and invasion of HCC cells. In searching for novel ZNF281 regulated genes, RNA-seq was performed on BGI-seq500 platform using the obtained stable cells of Con, ZNF281.kd1 and ZNF281.kd2 in HLE background (each in duplicate). The criteria of log2 FC (fold change) >1.5, and q value <0.001 was set for calling differentially expressed genes (DEGs). Besides, to minimize the off-target effect of single shRNAs, only DEGs that show consistent trend of alteration (up-regulated or down-regulated in both ZNF281.kd1 and ZNF281.kd2 groups against control shRNA group) were selected as potential ZNF281 targets. A list of potential targets was identified, including both up-regulated and down-regulated genes upon ZNF281 depletion. Further mechanistic studies were performed to uncover transcriptional regulation of ZNF281 on these genes. Our study was supposed to be helpful for understanding the molecular mechanism underpinning progression of HCC, and might also hold therapeutic potential for HCC treatment.
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Project description:Background & Aims: Aberrant activation of fatty acid synthase (FASN) is a major metabolic event during the development of HCC. We evaluated the therapeutic efficacy of TVB3664, a novel FASN inhibitor, either alone or in combination, for HCC treatment. Approach & Results: The therapeutic efficacy and the molecular pathways targeted by TVB3664, either alone or with tyrosine kinase inhibitors or the checkpoint inhibitor anti-PD-L1 antibody, were assessed in human HCC cell lines and multiple oncogene-driven HCC mouse models. RNAseq was performed to characterize the global gene expression and metabolic profiles. TVB3664 effectively ameliorated the fatty liver phenotype in the aged mice and AKT activation-induced hepatic steatosis. TVB3664 monotherapy showed moderate efficacy in NASH-related murine HCCs, induced by loss of PTEN and c-MET overexpression. TVB3664, in combination with cabozantinib, triggered tumor regression in this mouse HCC model but did not improve the responsiveness to immunotherapy. Global gene expression revealed that TVB3664 predominantly modulated metabolic processes, while TVB3664 synergized with cabozantinib to downregulate multiple cancer-related pathways, especially the AKT/mTOR pathway and cell proliferation genes. TVB3664 also improved the therapeutic efficacy of sorafenib and cabozantinib in the FASN-dependent c-MYC HCC model. However, TVB3664 had no efficacy nor synergistic effects in FASN-independent mouse HCC models. Conclusions: This preclinical study suggests the limited efficacy of targeting FASN as monotherapy for HCC treatment. However, FASN inhibitors could be combined with other drugs for improved effectiveness. These combination therapies could be developed based on the driver oncogenes, supporting precision medicine approaches for HCC treatment.
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Project description:siRNA-mediated inhibition compared to untreated cells and cells transfected with nonsense siRNA. Loss of contact inhibition and anchorage-independent growth are hallmarks of cancer cells. In this context, frequent inactivation of the Hippo pathway and subsequent nuclear enrichment of the transcriptional coactivator yes-associated protein (YAP) uncouple cell proliferation and anti-apoptosis from contact inhibition, associated with uncontrolled tumor growth and tumor cell dissemination. However, general molecular mechanisms of tumor-supporting YAP activity remain unclear. In this study, we show that overexpression and nuclear accumulation of YAP in hepatocytes and hepatocellular carcinoma (HCC) cells leads to an induction of the Notch pathways through transcriptional activation of the Notch ligand jagged-1 (Jag-1). This induction of Jag-1 strictly depends on binding of YAP to TEAD4 and does not rely on WNT/β-catenin pathway activity. Co-activation of YAP, TEAD4, Jag-1, and the Notch target gene Hes-1 was significantly higher in HCC from patients with poor prognosis. High-level expression and nuclear accumulation of YAP correlates with Jag-1/Notch activation not only in human HCC tissues, but also in colon and pancreatic cancer tissues. Thus, our data demonstrate that YAP-driven co-activation of the Jag-1/Notch pathway in part facilitates oncogenic properties of the oncogene YAP not only in HCC but also in different gastrointestinal malignancies. Expression profiling of untreated HCC cell lines (control 1), cells transfected with scrambled/nonsense siRNA (control 2), and after siRNA-mediated YAP inhibition.
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