FAM83H-AS1 is a non-coding oncogenic driver and therapeutic target of lung adenocarcinoma
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ABSTRACT:
PROVIDER: PRJNA669700 | ENA |
REPOSITORIES: ENA
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Project description:Our study suggested that FAM83H-AS1 was a potential oncogenic driver due to chromosome 8q24 amplification in lung adenocarcinoma. To investigate the molecular mechanism of FAM83H-AS1, we performed high-thoughput RNA sequencing (RNA-Seq) assays after the silence of FAM83H-AS1 in A549 cell lines.
2020-10-20 | GSE159559 | GEO
Project description:Human papillomavirus 42 is an oncogenic driver in Digital Papillary Adenocarcinoma.
| PRJNA803904 | ENA
Project description:Objectives: Long non-coding RNAs (lncRNAs) have been shown to play important roles in the development and progression of cancer. However, functional lncRNAs and their downstream mechanisms are largely unknown in the molecular pathogenesis of esophageal adenocarcinoma (EAC) and its progression. Design: lncRNAs that are abnormally upregulated in EACs were identified by RNA-seq analysis, followed by quantitative RT-PCR (qRTPCR) validation using tissues from 31 EAC patients. Cell biological assays in combination with siRNA-mediated knockdown were performed in order to probe the functional relevance of these lncRNAs. Results: We discovered that a lncRNA, HNF1A-AS1, is markedly upregulated in human primary EACs relative to their corresponding normal esophageal tissues (mean fold change 7.2, p<0.01). We further discovered that HNF1A-AS1 knockdown significantly inhibited cell proliferation and anchorage independent growth, suppressed S-phase entry, and inhibited cell migration and invasion in multiple in vitro EAC models (p<0.05). A gene ontological analysis revealed that HNF1A-AS1 knockdown preferentially affected genes that are linked to assembly of chromatin and the nucleosome, a mechanism essential to cell cycle progression. The well-known cancer-related lncRNA, H19, was the gene most markedly inhibited by HNF1A-AS1 knockdown. Consistent to this finding, there was a significant positive correlation between HNF1A-AS1 and H19 expression in primary EACs (p<0.01). In order to identify novel oncogenic lncRNAs in esophageal adenocarcinogenesis, we carried out RNA-seq of a matched NE-BE-EAC tissue pair
2013-10-21 | E-GEOD-48240 | biostudies-arrayexpress
Project description:BackgroundLittle is known about noncoding oncogenes of lung adenocarcinoma (LUAD), and these potential drivers might provide novel therapeutic targets.MethodsSince abnormally overexpression of oncogenic drivers is induced by genomic variation, we here utilized genomic, transcriptomic, and clinical prognosis data of The Cancer Genome Atlas (TCGA) LUAD datasets to discover novel drivers from long noncoding RNAs. We further used zebrafish models to validate the biological function of candidates in vivo. The full length of FAM83H-AS1 was obtained by rapid amplification of the cDNA ends assay. RNA pull-down, RNA immunoprecipitation, quantitative mass spectrometry, and RNA sequencing assays were conducted to explore the potential mechanisms. Additionally, we used CRISPR interference (CRISPRi) method and patient-derived tumor xenograft (PDTX) model to evaluate the therapeutic potential of targeting FAM83H-AS1.ResultsThe results suggest that FAM83H-AS1 is a potential oncogenic driver due to chromosome 8q24 amplification. Upregulation of FAM83H-AS1 results in poor prognosis of LUAD patients in both Jiangsu Cancer Hospital (JSCH) and TCGA cohorts. Functional assays revealed that FAM83H-AS1 promotes malignant progression and inhibits apoptosis. Mechanistically, FAM83H-AS1 binds HNRNPK to enhance the translation of antiapoptotic oncogenes RAB8B and RAB14. Experiments using CRISPRi-mediated xenografts and PDTX models indicated that targeting FAM83H-AS1 inhibited LUAD progression in vivo.ConclusionsOur work demonstrates that FAM83H-AS1 is a noncoding oncogenic driver that inhibits LUAD apoptosis via the FAM83H-AS1-HNRNPK-RAB8B/RAB14 axis, which highlights the importance and potential roles that FAM83H-AS1 may serve as a novel therapeutic target for LUAD.
| S-EPMC7882096 | biostudies-literature
Project description:Human papillomavirus 42 is an oncogenic driver in Digital Papillary Adenocarcinoma [full_genomes]
| PRJNA803907 | ENA
Project description:Human papillomavirus 42 is an oncogenic driver in Digital Papillary Adenocarcinoma [tumors]
| PRJNA803909 | ENA
Project description:Human papillomavirus 42 is an oncogenic driver in Digital Papillary Adenocarcinoma [transductions]
| PRJNA803908 | ENA
Project description:The skin serves as a barrier to the environment and is constantly exposed to viral pathogens. However, whether and how viral pathogens contribute to oncogenesis of rare skin cancers has not been explored. We analyzed 18 skin cancers by exploiting sparse off-target reads from commonly available next-generation sequencing data and identify human papillomavirus 42 (HPV42) reads in digital papillary adenocarcinoma (DPA). We show that HPV42 recapitulates the molecular hallmarks of oncogenic HPVs and shares a conserved transcriptomic fingerprint of HPV-transformation. Finally, we show that HPV42 relies on established cellular targets of oncogenic HPVs for its transforming activity. The discovery of HPV42 as a novel oncogenic driver highlights the utility of next-generation sequencing data for the discovery of novel pathogen-disease associations and suggests expansion of current HPV vaccination programs to reduce the cancer burden in humans.
2022-10-10 | GSE196217 | GEO
Project description:The skin serves as a barrier to the environment and is constantly exposed to viral pathogens. However, whether and how viral pathogens contribute to oncogenesis of rare skin cancers has not been explored. We analyzed 18 skin cancers by exploiting sparse off-target reads from commonly available next-generation sequencing data and identify human papillomavirus 42 (HPV42) reads in digital papillary adenocarcinoma (DPA). We show that HPV42 recapitulates the molecular hallmarks of oncogenic HPVs and shares a conserved transcriptomic fingerprint of HPV-transformation. Finally, we show that HPV42 relies on established cellular targets of oncogenic HPVs for its transforming activity. The discovery of HPV42 as a novel oncogenic driver highlights the utility of next-generation sequencing data for the discovery of novel pathogen-disease associations and suggests expansion of current HPV vaccination programs to reduce the cancer burden in humans.
2022-10-10 | GSE196216 | GEO
Project description:The skin serves as a barrier to the environment and is constantly exposed to viral pathogens. However, whether and how viral pathogens contribute to oncogenesis of rare skin cancers has not been explored. We analyzed 18 skin cancers by exploiting sparse off-target reads from commonly available next-generation sequencing data and identify human papillomavirus 42 (HPV42) reads in digital papillary adenocarcinoma (DPA). We show that HPV42 recapitulates the molecular hallmarks of oncogenic HPVs and shares a conserved transcriptomic fingerprint of HPV-transformation. Finally, we show that HPV42 relies on established cellular targets of oncogenic HPVs for its transforming activity. The discovery of HPV42 as a novel oncogenic driver highlights the utility of next-generation sequencing data for the discovery of novel pathogen-disease associations and suggests expansion of current HPV vaccination programs to reduce the cancer burden in humans.
2022-10-10 | GSE196215 | GEO