Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA283316 | ENA |
REPOSITORIES: ENA
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Project description:Epigenetic regulators are attractive targets for the development of new cancer therapies. Among them, the ATP-dependent chromatin remodeling complexes control the chromatin architecture and play important roles in gene regulation. They are often found to be mutated and de-regulated in cancers, but how they influence the cancer gene expression program during cancer initiation and progression is not fully understood. Here we show that the INO80 chromatin remodeling complex is required for oncogenic transcription and tumor growth in non-small cell lung cancer (NSCLC). Ino80, the SWI/SNF ATPase in the complex, is highly expressed in NSCLC cells compared to normal lung epithelia cells. Further, its expression, as well as that of another subunit Ino80b, negatively correlates with disease prognosis in lung cancer patients. Functionally, Ino80 silencing inhibits NSCLC cell proliferation and anchorage-independent growth in vitro and tumor formation in mouse xenografts. It occupies enhancer regions near lung cancer-associated genes, and its occupancy correlates with increased genome accessibility and enhanced expression of downstream genes. Together, our study defines a critical role of INO80 in promoting oncogenic transcription and NSCLC tumorigenesis, and reveals a potential treatment strategy for inhibiting the cancer transcription network by targeting the INO80 chromatin remodeling complex. Human lung cancer cell line A549 cells were infected with shNT or shIno80, and total RNA was extracted 4 days after infection. The RNA was submitted to RNA-Seq subsequently. For ChIP-Seq, A549 infected with shNT or shIno80, was used for ChIP-Seq for corresponding factors.
2016-08-03 | E-GEOD-85117 | biostudies-arrayexpress
Project description:The INO80 chromatin remodeling complex regulates the gene expression (no stress)
| PRJNA278168 | ENA
Project description:Epigenetic regulators are attractive targets for the development of new cancer therapies. Among them, the ATP-dependent chromatin remodeling complexes control the chromatin architecture and play important roles in gene regulation. They are often found to be mutated and de-regulated in cancers, but how they influence the cancer gene expression program during cancer initiation and progression is not fully understood. Here we show that the INO80 chromatin remodeling complex is required for oncogenic transcription and tumor growth in non-small cell lung cancer (NSCLC). Ino80, the SWI/SNF ATPase in the complex, is highly expressed in NSCLC cells compared to normal lung epithelia cells. Further, its expression, as well as that of another subunit Ino80b, negatively correlates with disease prognosis in lung cancer patients. Functionally, Ino80 silencing inhibits NSCLC cell proliferation and anchorage-independent growth in vitro and tumor formation in mouse xenografts. It occupies enhancer regions near lung cancer-associated genes, and its occupancy correlates with increased genome accessibility and enhanced expression of downstream genes. Together, our study defines a critical role of INO80 in promoting oncogenic transcription and NSCLC tumorigenesis, and reveals a potential treatment strategy for inhibiting the cancer transcription network by targeting the INO80 chromatin remodeling complex. Human lung cancer cell line A549 cells were infected with shNT or shIno80, and total RNA was extracted 4 days after infection. The RNA was submitted to RNA-Seq subsequently. For ChIP-Seq, A549 infected with shNT or shIno80, was used for ChIP-Seq for corresponding factors.
2016-08-03 | E-GEOD-85118 | biostudies-arrayexpress
Project description:The INO80 chromatin remodeling complex regulates the gene expression under oxidative stress condtion (stress)
| PRJNA278167 | ENA
Project description:Epigenetic regulators are attractive targets for the development of new cancer therapies. Among them, the ATP-dependent chromatin remodeling complexes control the chromatin architecture and play important roles in gene regulation. They are often found to be mutated and de-regulated in cancers, but how they influence the cancer gene expression program during cancer initiation and progression is not fully understood. Here we show that the INO80 chromatin remodeling complex is required for oncogenic transcription and tumor growth in non-small cell lung cancer (NSCLC). Ino80, the SWI/SNF ATPase in the complex, is highly expressed in NSCLC cells compared to normal lung epithelia cells. Further, its expression, as well as that of another subunit Ino80b, negatively correlates with disease prognosis in lung cancer patients. Functionally, Ino80 silencing inhibits NSCLC cell proliferation and anchorage-independent growth in vitro and tumor formation in mouse xenografts. It occupies enhancer regions near lung cancer-associated genes, and its occupancy correlates with increased genome accessibility and enhanced expression of downstream genes. Together, our study defines a critical role of INO80 in promoting oncogenic transcription and NSCLC tumorigenesis, and reveals a potential treatment strategy for inhibiting the cancer transcription network by targeting the INO80 chromatin remodeling complex.
2016-08-03 | GSE85117 | GEO
Project description:We report the high-throughput profiling of INO80 knockdown by siRNA in human kidney-2 cells (HK-2). We found that downstream target genes of INO80. This study provides novel insights into the chromatin remodeling factors regulated by INO80 in renal epithelial cells.
2023-08-23 | GSE224479 | GEO
Project description:During transcription, nucleosomes are evicted from regulatory and coding regions yet chromatin structure is stable. Restoration of chromatin structure involves concerted action of chromatin modifying activities. Our analysis demonstrates a genome wide function of the INO80 remodeling complex for stable repositioning of the nucleosome immediately proximal to the transcription initiation site. INO80 dependent remodeling of the promoter proximal nucleosomes has a global repressive role. Recruitment of INO80 to proximal nucleosomes overlaps with the elongating Polymerase II complex assembly. The amount of associated Polymerase II at start sites correlates with INO80 recruitment for inducible and constantly transcribed genes. Furthermore, at highly inducible promoters INO80 is required for repression of bidirectional transcription. Therefore, we suggest a function for INO80 after transcription initiation to achieve Polymerase II dependent reassembly of promoter proximal nucleosomes.
2016-12-24 | E-MTAB-1810 | biostudies-arrayexpress
Project description:INO80 is involved in many chromatin-dependent functions. However, its role in pluripotency has not been fully defined. We examined the impact of Ino80 deletion in the naïve and primed pluripotent stem cells. We found that Ino80 deletion had minimal effect on self-renewal and gene expression in the naïve state, but led to cellular differentiation and de-repression of developmental genes in the primed state. Mechanistically, INO80 co-occupied gene promoters that were bivalently marked by H3K4me3 and H3K27me3. Further, its occupancy was required for H3K27me3 installation and maintenance, as well as downstream gene repression. Finally, INO80 promoted H2A.Z occupancy at the bivalent domains, which in turn facilitated the polycomb repressive complex 2 (PRC2) recruitment. Together, our results identified the INO80-H2A.Z axis as an essential step for bivalent chromatin and poised gene expression and uncovered an epigenetic mechanism by which chromatin remodeling, histone variant, and histone modification coordinately control cell fate.
2021-07-04 | GSE158528 | GEO
Project description:INO80 is involved in many chromatin-dependent functions. However, its role in pluripotency has not been fully defined. We examined the impact of Ino80 deletion in the naïve and primed pluripotent stem cells. We found that Ino80 deletion had minimal effect on self-renewal and gene expression in the naïve state, but led to cellular differentiation and de-repression of developmental genes in the primed state. Mechanistically, INO80 co-occupied gene promoters that were bivalently marked by H3K4me3 and H3K27me3. Further, its occupancy was required for H3K27me3 installation and maintenance, as well as downstream gene repression. Finally, INO80 promoted H2A.Z occupancy at the bivalent domains, which in turn facilitated the polycomb repressive complex 2 (PRC2) recruitment. Together, our results identified the INO80-H2A.Z axis as an essential step for bivalent chromatin and poised gene expression and uncovered an epigenetic mechanism by which chromatin remodeling, histone variant, and histone modification coordinately control cell fate.
2021-07-04 | GSE158537 | GEO
Project description:INO80 is involved in many chromatin-dependent functions. However, its role in pluripotency has not been fully defined. We examined the impact of Ino80 deletion in the naïve and primed pluripotent stem cells. We found that Ino80 deletion had minimal effect on self-renewal and gene expression in the naïve state, but led to cellular differentiation and de-repression of developmental genes in the primed state. Mechanistically, INO80 co-occupied gene promoters that were bivalently marked by H3K4me3 and H3K27me3. Further, its occupancy was required for H3K27me3 installation and maintenance, as well as downstream gene repression. Finally, INO80 promoted H2A.Z occupancy at the bivalent domains, which in turn facilitated the polycomb repressive complex 2 (PRC2) recruitment. Together, our results identified the INO80-H2A.Z axis as an essential step for bivalent chromatin and poised gene expression and uncovered an epigenetic mechanism by which chromatin remodeling, histone variant, and histone modification coordinately control cell fate.
2021-07-04 | GSE158533 | GEO