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KIMAT1 and HIF1A-As2 silencing small RNA-seq

ABSTRACT: In our study, we valided the important oncogeneic roles of KIMAT1 and HIF1A-As2 in non-small cell lung cancer. We used custom designed GapmeRs to silence the KIMAT1 and HIF1A-As2 in H1299 and performed small RNA-seq. 214 and 233 microRNAs were regulated by KIMAT1 and HIF1A-As2, respectively.

ORGANISM(S): Homo sapiens

PROVIDER: GSE124629 | GEO | 2020/12/17

REPOSITORIES: GEO

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KIMAT1 and HIF1A-As2 silencing RNA-seq

Project description:In our study, we valided the important oncogeneic roles of KIMAT1 and HIF1A-As2 in non-small cell lung cancer. We used custom designed GapmeRs to silence the KIMAT1 and HIF1A-As2 in H1299 and performed RNA-seq. 11389 and 7767 genes were regulated by KIMAT1 and HIF1A-As2, respectively.

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KIMAT1 and HIF1A-As2 silencing small RNA-seq

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Project description:AS2 encode AS2-domain containing protein and may regulate transcription. AS2 is involved in the determination of axes of leaves of Arabidopsis thaliana. Type IB DNA topoisomerase (TOP1α) gene has genetic interaction with AS1 and AS2 and is involved in repression of leaf polarity genes. To know the gene regulation in the leaf development, expression profile among wild-type and as2 mutant treated with and without 10-hydroxyl substituted camptothecin (10H-CPT), a specific TOP1 inhibitor, were compared

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Project description:AS2 encodes a protein containing AS2 domain and epigenetically regulate transcription. RH10 encodes an ortholog of human DEAD-box RNA helicase DDX47. These genes are involved in the formation of axes of leaves of Arabidopsis thaliana. To know the gene regulation in the leaf development, expression profile among wild-type, as2, rh10 and as2 rh10 double mutant plants were compared.

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Stenotrophomonas sp. AS2

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Chromatin states in glioblastoma stem cells (HOXA-AS2 depletion)

Project description:Glioblastoma multiform account for about half of all gliomas and are the most deadly and aggressive forms. Its therapeutic resistance and tumor relapse rely on a subpopulation of cells, the so-called Glioma-stem Cells (GSCs). Here, we investigated for the role of the long non-coding RNA HOXA-AS2 in GSC biology by conducting descriptive and functional analyses of glioma samples classified according to their isocitrate dehydrogenase (IDH1) gene mutation status, and of glioma stem cells. We found that HOXA-AS2 is overexpressed only in aggressive (IDHwt) glioma and GSC. Sh-RNA-based depletion of HOXA-AS2 affects GSC both at the cellular and molecular levels with a decrease in proliferation and altered expression of several hundreds of their genes. Integrative analysis revealed that these changes is expression are not associated to changes in DNA methylation or chromatin signature at the promoter of most deregulated genes following HOXA-AS2 silencing in GSC, supporting a post-transcriptional regulation. In addition, transcription factor motif enrichment and correlation analyses sustained that HOXA-AS2 affect, directly or indirectly, expression of key transcription factors of GCS biology, including E2F8, E2F1, STAT1 and ATF3 to, in fine, contributes to their pathological status by promoting proliferation and modulating the inflammation pathway of Glioma Stem Cell.

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Project description:The underlying mechanisms of long non-coding RNAs (lncRNA) participating in the progression of lung cancers are largely unknown. We found a novel lncRNA, PIK3CD antisense RNA 2 (PIK3CD-AS2), that contributes to lung adenocarcinoma (LUAD) progression. The expression characteristics of PIK3CD-AS2 in LUAD were analyzed using microarray expression profile, The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) datasets, and validated in 92 paired LUAD tissues by chromogenic in situ hybridization. Our data confirmed that PIK3CD-AS2 expression is a crucial regulator of LUAD progression and associated with shorter patient survival. In vitro studies showed that PIK3CD-AS2 increased cell growth and slowed apoptosis in p53wt cells but not in p53null cells. Mechanically, it is demonstrated that PIK3CD-AS2 bound to and maintained the stability of Y-box binding protein 1 (YBX1), a potent destabilizer of p53, by impeding its ubiquitination and degradation. Downexpression of YBX1 reversed PIK3CD-AS2-mediated inhibition of p53 signaling. Additionally, the therapeutic effect evaluation of a Locked Nuclear Acid (LNA) specifically targeting PIK3CD-AS2 showed an anti-tumor activity in mice with A549 cells xenograft and p53 wild-type LUAD patient-derived tumor xenograft (PDTX) model. Clinically, the high expression of PIK3CD-AS2 showed a poor disease-free survival in p53 wild-type patients in TCGA database. Our findings suggest that PIK3CD-AS2 regulates LUAD progression and elucidate a new PIK3CD-AS2/YBX1/p53 signaling axis, providing a potential lncRNA-directed therapeutic strategy especially in p53 wild-type LUAD patients.

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