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Epigenetic enigma: reinstating normalcy at a naïve chromosomal locus by suppressing an oncogenic lncRNA transgene

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE249606 | GEO | 2025/06/23

REPOSITORIES: GEO

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Epigenetic enigma: reinstating normalcy at a naïve chromosomal locus by suppressing an oncogenic lncRNA transgene [Bisulfite-Seq]

Project description:Maintaining genome integrity is crucial for the proper functioning and development of organisms. One intriguing aspect of genome integrity is the formation and function of neocentromeres at non-centromeric sites. The centromere-specific protein CENP-A plays a vital role in centromere identification and function. However, in many cancers, CENP-A is often found to be ectopically misplaced when overexpressed. Moreover, the deposition of CENP-A at the centromere depends on the transcription of centromeric non-coding RNAs. Consequently, ectopic CENP-A is found at transcriptionally active and frequent breakpoint regions. To further explore the ectopic CENP-A localization, we engineered a stable ectopic CENP-A site at a naïve chromosome by overexpressing a non-centromeric oncogenic lncRNA capable of recruiting CENP-A to its transcription site. We tracked cells carrying the stable transgene to understand the stability and longevity of the induced ectopic CENP-A site and the harboring chromosome. Our findings revealed that the induced epigenetic memory was eventually lost by suppression of the transgene through competing epigenetic silencing mechanisms. This epigenetic restoration naturally reversed the ectopic CENP-A level to its previous levels at the engineered site. Our observations suggest that cells may have evolved failsafe mechanisms to prevent neocentromere formation at ectopic sites unless otherwise favored by selection involving multiple components.

2025-06-23 | GSE249602 | GEO

Epigenetic enigma: reinstating normalcy at a naïve chromosomal locus by suppressing an oncogenic lncRNA transgene [WGS]

2025-06-23 | GSE249599 | GEO

Epigenetic enigma: reinstating normalcy at a naïve chromosomal locus by suppressing an oncogenic lncRNA transgene

Project description:Epigenetic enigma: reinstating normalcy at a naïve chromosomal locus by suppressing an oncogenic lncRNA transgene

| PRJNA1049797 | ENA

Epigenetic enigma: reinstating normalcy at a naïve chromosomal locus by suppressing an oncogenic lncRNA transgene [WGS]

Project description:Epigenetic enigma: reinstating normalcy at a naïve chromosomal locus by suppressing an oncogenic lncRNA transgene [WGS]

| PRJNA1049791 | ENA

Epigenetic enigma: reinstating normalcy at a naïve chromosomal locus by suppressing an oncogenic lncRNA transgene [Bisulfite-Seq]

Project description:Epigenetic enigma: reinstating normalcy at a naïve chromosomal locus by suppressing an oncogenic lncRNA transgene [Bisulfite-Seq]

| PRJNA1049799 | ENA

Oncogenic lncRNAs alter epigenetic memory at a fragile chromosomal site in human cancer cells.

Project description:Chromosome instability is a critical event in cancer progression. Histone H3 variant CENP-A plays a fundamental role in defining centromere identity, structure, and function but is innately overexpressed in several types of solid cancers. In the cancer background, excess CENP-A is deposited ectopically on chromosome arms, including 8q24/cMYC locus, by invading transcription-coupled H3.3 chaperone pathways. Up-regulation of lncRNAs in many cancers correlates with poor prognosis and recurrence in patients. We report that transcription of 8q24-derived oncogenic lncRNAs plays an unanticipated role in altering the 8q24 chromatin landscape by H3.3 chaperone-mediated deposition of CENP-A-associated complexes. Furthermore, a transgene cassette carrying specific 8q24-derived lncRNA integrated into a naïve chromosome locus recruits CENP-A to the new location in a cis-acting manner. These data provide a plausible mechanistic link between locus-specific oncogenic lncRNAs, aberrant local chromatin structure, and the generation of new epigenetic memory at a fragile site in human cancer cells.

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Oncogenic Myc translocations are independent of chromosomal location and orientation of the immunoglobulin heavy chain locus.

Project description:Many tumors are characterized by recurrent translocations between a tissue-specific gene and a proto-oncogene. The juxtaposition of the Ig heavy chain gene and Myc in Burkitt's lymphoma and in murine plasmacytoma is a classic example. Regulatory elements within the heavy chain constant region locus are required for Myc translocation and/or deregulation. However, many genes are regulated by cis-acting elements at distances up to 1,000 kb outside the locus. Such putative distal elements have not been examined for the heavy chain locus, particularly in the context of Myc translocations. We demonstrate that a transgene containing the Ig heavy chain constant region locus, inserted into five different chromosomal locations, can undergo translocations involving Myc. Furthermore, these translocations are able to generate plasmacytomas in each transgenic line. We conclude that the heavy chain constant region locus itself includes all of the elements necessary for both the translocation and the deregulation of the proto-oncogene.

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Project description:We characterized the epigenetic landscape of genes encoding long noncoding RNAs (lncRNAs) across 6,475 tumors and 455 cancer cell lines. In stark contrast to the CpG island hypermethylation phenotype in cancer, we observed a recurrent hypomethylation of 1,006 lncRNA genes in cancer, including EPIC1 (epigenetically-induced lncRNA1). Overexpression of EPIC1 is associated with poor prognosis in luminal B breast cancer patients and enhances tumor growth in vitro and in vivo. Mechanistically, EPIC1 promotes cell-cycle progression by interacting with MYC through EPIC1's 129-283 nt region. EPIC1 knockdown reduces the occupancy of MYC to its target genes (e.g., CDKN1A, CCNA2, CDC20, and CDC45). MYC depletion abolishes EPIC1's regulation of MYC target and luminal breast cancer tumorigenesis in vitro and in vivo.

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Sexually Dimorphic Expression of eGFP Transgene in the Akr1A1 Locus of Mouse Liver Regulated by Sex Hormone-Related Epigenetic Remodeling.

Project description:Sexually dimorphic gene expression is commonly found in the liver, and many of these genes are linked to different incidences of liver diseases between sexes. However, the mechanism of sexually dimorphic expression is still not fully understood. In this study, a pCAG-eGFP transgenic mouse strain with a specific transgene integration site in the Akr1A1 locus presented male-biased EGFP expression in the liver, and the expression was activated by testosterone during puberty. The integration of the pCAG-eGFP transgene altered the epigenetic regulation of the adjacent chromatin, including increased binding of STAT5b, a sexually dimorphic expression regulator, and the transformation of DNA methylation from hypermethylation into male-biased hypomethylation. Through this de novo sexually dimorphic expression of the transgene, the Akr1A1(eGFP) mouse provides a useful model to study the mechanisms and the dynamic changes of sexually dimorphic gene expression during either development or pathogenesis of the liver.

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A dispensable Plasmodium locus for stable transgene expression.

Project description:The ribosomal small subunit locus has been used for transgene expression in the rodent malaria parasites, Plasmodium berghei and Plasmodium yoelii, but this strategy utilizes single crossover integration and is thus prone to reversion by plasmid excision. Targeting of the ribosomal subunit locus may also have a negative effect on oocyst development in the mosquito. In P. berghei, the p230 paralog locus has been used for transgene expression. Here, we show that the P. yoelii S1 locus (sporozoite expressed gene 1) (PY05712) is dispensable and can be used for stable transgene expression throughout the parasite life cycle. P. yoelii s1(-) parasites show no defect in blood stage replication, oocyst formation, sporozoite production, or liver stage development when compared to P. yoelii wildtype parasites. Further, we show that a fluorescent transgene can be stably expressed from this site. This demonstrates that the S1 locus can be utilized for stable expression of heterologous genes in rodent malaria parasites.

| S-EPMC2839042 | biostudies-literature

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