FAM83H-AS1 is a non-coding oncogenic driver and therapeutic target of lung adenocarcinoma
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ABSTRACT:
PROVIDER: PRJNA669700 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12831457.fastq.gz | Fastqsanger.gz | |||
| SRR12831458.fastq.gz | Fastqsanger.gz | |||
| SRR12831459.fastq.gz | Fastqsanger.gz | |||
| SRR12831460.fastq.gz | Fastqsanger.gz | |||
| SRR12831461.fastq.gz | Fastqsanger.gz |
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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:We silenced FAM83H-AS1 shRNAs in cell line MCF7 carried a ~75% silencing compared to thenegative control (NC). We evaluated the role of FAM83H-AS1 on oncogenic phenotypes in the MCF7 breast cancer cell line model. The knockdown of FAM83H-AS1 was achieved with ~75% of silencing efficiency. A complete transcriptomic analysis after silencing of FAM83H-AS1 revealed an impact on the global expression.
2020-12-12 | GSE135466 | GEO
Project description:To investigate the role of lncRNA FAM83H-AS1 in breast cancer, we used shRNA to silence FAM83H-AS1 in MDA-MB-468 cells and performed RNA-seq analysis.
2026-02-01 | GSE289922 | GEO
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:FAM83H-AS1 silencing in MCF7 breast cancer cells
| PRJNA558978 | ENA
Project description:ObjectiveOvarian cancer (OC) is one of the most aggressive women cancers with increasing incidence and mortality rates worldwide. Long non-coding RNAs (lncRNAs) could as major players in OC process. Although FAM83H antisense RNA1 (FAM83H-AS1) is demonstrated play an important roles in a many cancers, the detailed function and mechanism has not been reported in OC.ResultsWe integrated multiple kinds of bioinformatics approaches and experiments validated method to evaluate functions of FAM83H-AS1 in OC. Some differential expressed lncRNAs were identified between OC and normal control tissues. FAM83H-AS1 was one of most differentially expressed lncRNAs and up-regulated in multiple cancer types. Specially, expression of FAM83H-AS1 was higher in OC and showed difference in diverse stages. High FAM83H-AS1 expression is associated with worse pan-cancer and OC outcomes. FAM83H-AS1-centric network including lncRNA-miRNA, lncRNA-protein and lncRNA-mRNA ceRNA network were constructed to infer the function and mechanism of FAM83H-AS1. There were two methylation sites including cg01399317 and cg20519035 located at FAM83H-AS1. The methylation level of cg01399317 was correlated with gene expression of FAM83H-AS1. The expression level of FAM83H-AS1 was correlated with infiltration level of immune cell including macrophage, neutrphil and dendritic cell in OC patients. Lastly, qRT-PCR showed that the expression of FAM83H-AS1 was higher in OC tissues than normal control tissues.ConclusionCollectively, these results indicated that FAM83H-AS1 may act as an oncogenic driver and it may be a potential therapy target in OC.
| S-EPMC7792319 | biostudies-literature
Project description:Effect of FAM83H-AS1 knockdown in MDA-MB-468 cells [cellseq]
| PRJNA1225303 | 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:We generated Fam83h-deficient mice (Fam83hem2(IMPC)Ccpcz, Fam83h-/-) and mice lacking a part of N-terminal CK1-binding domain (Fam83h∆87/∆87). Co-IP with anti-FAM83H antibody has confirmed the FAM83H–CK1 interaction in Fam83hwt/wt samples, which was absent in Fam83h-/- lysates. Additionally, samples from Fam83hΔ87/Δ87 mice were less likely to show FAM83H–CK1 interaction. Similarly, when CK1a antibody was used for pull downs, FAM83H–CK1 interaction was observed in Fam83hwt/wt lysates , but not in Fam83h-/- and Fam83hΔ87/Δ87 samples.
2025-09-08 | PXD064193 | Pride
Project description:Truncation mutations in family with sequence similarity, member H (FAM83H) gene cause autosomal dominant hypocalcified amelogenesis imperfecta (ADHCAI). The aim of this study was to explore the effects of truncated FAM83H on enamel development. High throughput RNA-sequencing was used to detect the dysregulated signaling pathways in Fam83h-mutated LS8 cells. According to mRNA-sequencing, pathway related to cell adhesion was the most notably clustered in Fam83h-mutated cells. Immunofluorescence analysis further revealed decreased protein expression of desmoglein 3, a component of desmosomes, in Fam83h-mutated cells.
2024-01-28 | GSE195645 | GEO