Project description:To identify the novel tumor suppressors in hepatocellular carcinoma (HCC), we have employed whole genome microarray expression profiling as a discovery platform in HCC and paired normal liver tissues to identify genes which down-regulated in HCC. Among which, INTS6 and its pseudogene, namely INTS6P1, were found to be dramatically down-regulated in HCC. The down-regulated expression of INTS6 and INTS6P1 in HCC was further confirmed by real-time PCR. RNA was extracted from 3 pairs of HCC and normal liver tissue harvested from patients to undergo microarray study.
Project description:To identify the novel tumor suppressors in hepatocellular carcinoma (HCC), we have employed whole genome microarray expression profiling as a discovery platform in HCC and paired normal liver tissues to identify genes which down-regulated in HCC. Among which, INTS6 and its pseudogene, namely INTS6P1, were found to be dramatically down-regulated in HCC. The down-regulated expression of INTS6 and INTS6P1 in HCC was further confirmed by real-time PCR. RNA was extracted from 3 pairs of HCC and normal liver tissue harvested from patients to undergo microarray study.
Project description:To identify the novel tumor suppressors in hepatocellular carcinoma (HCC), we have employed whole genome microarray expression profiling as a discovery platform in HCC and paired normal liver tissues to identify genes which down-regulated in HCC. Among which, INTS6 and its pseudogene, namely INTS6P1, were found to be dramatically down-regulated in HCC. The down-regulated expression of INTS6 and INTS6P1 in HCC was further confirmed by real-time PCR.
Project description:To identify the novel tumor suppressors in hepatocellular carcinoma (HCC), we have employed whole genome microarray expression profiling as a discovery platform in HCC and paired normal liver tissues to identify genes which down-regulated in HCC. Among which, INTS6 and its pseudogene, namely INTS6P1, were found to be dramatically down-regulated in HCC. The down-regulated expression of INTS6 and INTS6P1 in HCC was further confirmed by real-time PCR.
Project description:Hepatocellular carcinoma (HCC) remains a significant clinical challenge due to limited diagnostic and therapeutic options. Non-coding RNAs, such as microRNAs (miRNAs), play key roles in cancer biology. Our previous findings showed that miR-423-5p exerts anti-cancer effects on HCC patients treated with sorafenib by promoting autophagy. In this study, we investigated the molecular mechanisms underlying its activity by generating SNU-387 HCC cell line stably overexpressing miR-423-5p and conducting a comprehensive proteomic analysis. Mass spectrometry profiling identified 698 differentially expressed proteins (DEPs) in miR-423-5p-overexpressing cells compared to controls. Functional enrichment analysis revealed significant alterations in metabolic pathways, particularly purine/pyrimidine metabolism and gluconeogenesis. To relate these findings to clinical context, we integrated experimentally validated and predicted miR-423-5p targets with The Cancer Genome Atlas (TCGA) Liver Hepatocellular Carcinoma (LIHC) dataset. Seven candidate proteins were significantly associated with patient prognosis (log-rank p < 0.05 for both overall and disease-free survival). These targets were downregulated in our miR-423-5p model but found to be upregulated in stage III HCC tissues from TCGA data.
Project description:We report the application of miRNAs analysis in exosomes based on second-generation high-throughput sequencing. Plasma samples from 3 hepatocellular carcinoma patients and 3 healthy controls were collected, and exosomes were isolated by ultra-centrifugation. MiRNAs in exosomes were then extracted and high-throughput sequencing was performed.By comparing the sequencing data, we screened out differentially expressed miRNAs and validated them with qRT-PCR in exosome samples, establishing and verifying the diagnostic panel of hepatocellular carcinoma composed of miR-212-5p, miR-519b-3p, miR-1248 and miR-1250-5p.
Project description:Hepatocellular carcinoma (HCC) exhibits diverse aetiologies and molecular heterogeneities, with a median 5-year overall survival (OS) of less than 70% due to late diagnosis and high recurrence rates post-curative ablation or surgery. This study investigated the complex tumor microenvironment (TME) in HCC, emphasizing the interactions between various cell types and their role in disease recurrence. Using samples from the PLANet 1.0 cohort (NCT03267641), spatial transcriptomics were performed on 17 tissue samples from 4 patients, and bulk RNA-seq on multi-region tumour sectors from 91 patients. Analysis revealed extensive intra- and inter-tumour gene expression heterogeneity, identifying a specific subset of endothelial cells (ECs), INTS6+ ECs, enriched and spatially co-localized with tumour cells in primary tumours of recurrent cases. A significant ANGPTL4-SDC1 ligand-receptor interaction was found between INTS6+ ECs and tumour cells. Interestingly, INTS6+ ECs were enriched in histologically annotated microvascular invasion (MVI). These findings suggest novel therapeutic targets focusing on endothelial cell interactions within TME.
