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7. Spatial-Temporal Genome Regulation in Stress-Response and Cell-Fate Change

Author

Erenpreisa, Jekaterina, primary, Giuliani, Alessandro, additional, Yoshikawa, Kenichi, additional, Falk, Martin, additional, Hildenbrand, Georg, additional, Salmina, Kristine, additional, Freivalds, Talivaldis, additional, Vainshelbaum, Ninel, additional, Weidner, Jonas, additional, Sievers, Aaron, additional, Pilarczyk, Götz, additional, and Hausmann, Michael, additional

Published
2023
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10. Contributors

Author

Amer, Amal O., primary, Ávalos, Yenniffer, additional, Belyayev, Alexander, additional, Caution, Kyle, additional, Cenci, Simone, additional, Cecconi, Francesco, additional, Choksi, Swati, additional, Cianfanelli, Valentina, additional, Cook, Katherine L., additional, Clarke, Robert, additional, Cornet-Boyaka, Estelle, additional, Cragg, Mark S., additional, Dakhlallah, Duaa, additional, Erenpreisa, Jekaterina, additional, Esaki, Masatoshi, additional, Feun, Lynn G., additional, Fink, Mark Y., additional, Gottlieb, Roberta A., additional, Guo, Jessie Y., additional, Harimoto, Norifumi, additional, Harris, James, additional, Hayat, M.A., additional, Hayashi, Toshihiko, additional, Hernández-Cáceres, Maria P., additional, Ikegami, Toru, additional, Ikejima, Takashi, additional, Inashkina, Inna, additional, Itoh, Shinji, additional, Ivanov, Andrei I., additional, Kehrl, John H., additional, Kuo, M.T., additional, Lang, Tali, additional, Franco Leal, Raquel, additional, Liu, Zhenggang, additional, Lipatova, Zhanna, additional, Luo, Jia, additional, Maehara, Yoshihiko, additional, Manque, Patricio, additional, Markaki, Maria, additional, Matsumoto, Yoshihiro, additional, Metaxakis, Athansios, additional, MeKee-Muir, Olivia C., additional, Morselli, Eugenia, additional, Nabar, Neel R., additional, Nassif, Melissa, additional, Nguyen, Dao, additional, Pengo, Niccolò, additional, Protasoni, Margherita, additional, Russell, Ryan C., additional, Salmina, Kristine, additional, Savaraj, Niramol, additional, Segev, Nava, additional, Shi, Chong-Shan, additional, Shirabe, Ken, additional, Ramos Silva, Francesca A., additional, Snyder, Michelle L., additional, Sukkar, Maria B., additional, Taanman, Jan-Willem, additional, Tavernarakis, Nektarios, additional, Toledo, Lilian, additional, Toshima, Takeo, additional, Tsung, Allan, additional, Wangpaichitr, Medhi, additional, Weichseldorfer, Matthew R., additional, White, Theresa L., additional, Woelhbier, Ute, additional, Wu, Chunjing, additional, Yoshizumi, Tomoharu, additional, You, Min, additional, Zhang, Lemeng, additional, and Zhang, Yan, additional

Published
2017
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11. The Enigma of cancer resistance to treatment

Author

Erenpreisa, Jekaterina, Salmina, Kristine, Anatskaya, Olga, Vinogradov, Alexander, and Cragg, Mark Steven

Abstract

Polyploid giant cancer cells (PGCC) are evaluated by histopathologists for cancer diagnosis, yet their role in cancer is poorly understood. In this essay, we highlight a particular aspect of these cells in relation to genomic self-organisation and transcriptional networks with relevance to treatment resistance. Embodying dynamic restructuring of the genomic network, epigenome and microenvironment, through explorative adaptation in response to sublethal challenge these cells operate at the edge of chaos and order. This state is manifested through oscillations in opposing cell fate pathways, with accelerated senescence coupled to reprogramming and an atavistic shift towards phylogenetically ancient unicellular genetic programmes accessed through bivalent mediator genes. It recapitulates certain unicellular life-cycles in a cancer “life-cycle” which reciprocally connects the somatic mitotic cell cycle with the germline cycle of the PGCC., Organisms, Vol 5, No 2 (2022): Special Issue: Where is Science Going? Scenarios and Perspectives of Contemporary Technoscience

Published
2022
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28. DNA methylation of the <italic>Oct4A</italic> enhancers in embryonal carcinoma cells after etoposide treatment is associated with alternative splicing and altered pluripotency in reversibly senescent cells.

Author

Baryshev, Mikhail, Inashkina, Inna, Salmina, Kristine, Huna, Anda, Jackson, Thomas R, and Erenpreisa, Jekaterina

Abstract

The epigenetic mechanisms underlying chemoresistance in cancer cells resulting from drug-induced reversible senescence are poorly understood. Chemoresistant ESC-like embryonal carcinoma PA1 cells treated with etoposide (ETO) were previously found to undergo prolonged G2 arrest with transient p53-dependent upregulation of opposing fate regulators, p21CIP1 (senescence) and OCT4A (self-renewal). Here we report on the analysis of the DNA methylation state of the distal enhancer (DE) and proximal enhancer (PE) of the Oct4A gene during this dual response. When compared to non-treated controls the methylation level increased from 1.3% to 12.5% and from 3% to 19.4%, in the DE and PE respectively. It included CpG and non-CpG methylation, which was not chaotic but presented two patterns in each enhancer. Discorrelating with methylation of enhancers, the transcription of Oct4A increased, however, a strong expression of the splicing form Oct4B was also induced, along with down-regulation of the Oct4A partners of in the pluripotency/self-renewal network Sox2 and Lin28. WB demonstrated disjoining of the OCT4A protein from the chromatin-bound fraction. In survival clones, methylation of the DE was considerably erased, while some remnant of methylation of the PE was still observed. The alternative splicing for Oct4B was reduced, Oct4A level insignificantly decreased, while the expression of Sox2 and Lin28 recovered, all three became proportionally above the control. These findings indicate the involvement of the transient patterned methylation of the Oct4A enhancers and alternative splicing in the adaptive regulation of cell fate choice during the p53-dependant dual state of reversible senescence in ESC-like cancer stem cells. [ABSTRACT FROM AUTHOR]

Published
2018
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31. DNA methylation of the Oct4Aenhancers in embryonal carcinoma cells after etoposide treatment is associated with alternative splicing and altered pluripotency in reversibly senescent cells

Author

Baryshev, Mikhail, Inashkina, Inna, Salmina, Kristine, Huna, Anda, Jackson, Thomas R, and Erenpreisa, Jekaterina

Abstract

ABSTRACTThe epigenetic mechanisms underlying chemoresistance in cancer cells resulting from drug-induced reversible senescence are poorly understood. Chemoresistant ESC-like embryonal carcinoma PA1 cells treated with etoposide (ETO) were previously found to undergo prolonged G2 arrest with transient p53-dependent upregulation of opposing fate regulators, p21CIP1 (senescence) and OCT4A (self-renewal). Here we report on the analysis of the DNA methylation state of the distal enhancer (DE) and proximal enhancer (PE) of the Oct4Agene during this dual response. When compared to non–treated controls the methylation level increased from 1.3% to 12.5% and from 3% to 19.4%, in the DE and PE respectively. It included CpG and non-CpG methylation, which was not chaotic but presented two patterns in each enhancer. Discorrelating with methylation of enhancers, the transcription of Oct4Aincreased, however, a strong expression of the splicing form Oct4Bwas also induced, along with down-regulation of the Oct4Apartners of in the pluripotency/self-renewal network Sox2and Lin28. WB demonstrated disjoining of the OCT4A protein from the chromatin-bound fraction. In survival clones, methylation of the DE was considerably erased, while some remnant of methylation of the PE was still observed. The alternative splicing for Oct4Bwas reduced, Oct4Alevel insignificantly decreased, while the expression of Sox2and Lin28recovered, all three became proportionally above the control. These findings indicate the involvement of the transient patterned methylation of the Oct4Aenhancers and alternative splicing in the adaptive regulation of cell fate choice during the p53-dependant dual state of reversible senescence in ESC-like cancer stem cells.

Published
2018
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38. Identification of Three Clinically Relevant Borrelia burgdorferiSensu Lato Genospecies by PCR-Restriction Fragment Length Polymorphism Analysis of 16S-23S Ribosomal DNA Spacer Amplicons

Author

Ranka, Renate, Bormane, Antra, Salmina, Kristine, and Baumanis, Viesturs

Abstract

ABSTRACTWe report the results of a study of the prevalences of three clinically relevant Borrelia burgdorferisensu lato genospecies (Borrelia burgdorferisensu stricto, Borrelia afzelii, and Borrelia garinii) in 1,040 questing Ixodesticks from all regions of Latvia, where Lyme borreliosis is endemic. The prevalences of Borreliain Ixodes ricinusand Ixodes persulcatuswere 22.6 and 27.9%, respectively. Molecular typing of B. burgdorferifrom infected ticks was performed by restriction fragment length polymorphism (RFLP) analysis of PCR-amplified fragments of the 16S-23S (rrs-rrlA) rRNA intergenic spacer by using species-specific primers and subsequent sequencing. The dominant Borreliaspecies in both Ixodesspecies was B. afzelii.In addition, different restriction patterns of B. gariniiand B. afzeliiwere also identified. This study demonstrates that the 16S-23S rRNA PCR-RFLP typing method is simple, sensitive, and fast and that it allows one to differentiate among B. burgdorferispecies and subspecies with various degrees of pathogenic potential directly in ticks. These features are important in monitoring Lyme disease.

Published
2004
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40. When Three Isn't a Crowd: A Digyny Concept for Treatment-Resistant, Near-Triploid Human Cancers.

Author

Salmina, Kristine, Gerashchenko, Bogdan I., Hausmann, Michael, Vainshelbaum, Ninel M., Zayakin, Pawel, Erenpreiss, Juris, Freivalds, Talivaldis, Cragg, Mark S., and Erenpreisa, Jekaterina

Subjects
*CELL cycle, *LETHAL mutations, *KARYOTYPES, *MITOSIS, *HELA cells, *DNA repair, *TUMOR growth
Abstract

Near-triploid human tumors are frequently resistant to radio/chemotherapy through mechanisms that are unclear. We recently reported a tight association of male tumor triploidy with XXY karyotypes based on a meta-analysis of 15 tumor cohorts extracted from the Mitelman database. Here we provide a conceptual framework of the digyny-like origin of this karyotype based on the germline features of malignant tumors and adaptive capacity of digyny, which supports survival in adverse conditions. Studying how the recombinatorial reproduction via diploidy can be executed in primary cancer samples and HeLa cells after DNA damage, we report the first evidence that diploid and triploid cell sub-populations constitutively coexist and inter-change genomes via endoreduplicated polyploid cells generated through genotoxic challenge. We show that irradiated triploid HeLa cells can enter tripolar mitosis producing three diploid sub-subnuclei by segregation and pairwise fusions of whole genomes. Considering the upregulation of meiotic genes in tumors, we propose that the reconstructed diploid sub-cells can initiate pseudo-meiosis producing two "gametes" (diploid "maternal" and haploid "paternal") followed by digynic-like reconstitution of a triploid stemline that returns to mitotic cycling. This process ensures tumor survival and growth by (1) DNA repair and genetic variation, (2) protection against recessive lethal mutations using the third genome. [ABSTRACT FROM AUTHOR]

Published
2019
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42. The Role of the Meiotic Component in Reproduction of B-RAF-Mutated Melanoma : A Review and “Brainstorming” Session

Author

Pjanova, Dace, Vainshelbaum, Ninel M., Salmina, Kristine, and Erenpreisa, Jekaterina

Subjects
Medical
Abstract

The ectopic expression of cancer testis (CT) antigens and classic meiotic genes is characteristic and a hallmark of poor prognosis of melanoma disease. Here the potential mechanisms of meiotic influence on the cell and life cycle of malignant melanoma are reviewed in the genetic, epigenetic, and evolutionary aspects. The involved mutant B-RAF and N-RAS-induced senescence may be reversed by reprogramming, with stemness linked to meiotic landscape, possibly induced by DNA double-strand breaks at the mutual telomere hot spots. The induced by senescence mitotic slippage (reset of interphase from arrested metaphase) and resulting polyploidy trigger the meiotic ploidy cycle to function for effective DNA recombination repair, genome reduction, and escape of survivors, which enter the mitotic cycle again. The aberrant meiotic pathway in cancer is reviewed in the ancestral asexual variants; inverted meiosis is possible. The conundrum of cancer aneuploidy paradox, selection of fit clones, and the Muller’s Ratchet of inevitable accumulation of harmful mutations is discussed. The bioinformatic study of the densely connected protein interaction network of CT antigen expressed genes revealed the melanomagenesis attractor composed of PRAME and small MAGEA group in primary tumors as compared with B-RAF-mutant nevi, restructured stemness network; invasive melanoma further displays the leading role of SPANX CT antigen group; meiotic genes are expressed in all three tissue cohorts.

Published
2019

43. The role of meiotic cohesin REC8 in chromosome segregation in gamma irradiation-induced endopolyploid tumour cells.

Author

Erenpreisa J, Cragg MS, Salmina K, Hausmann M, and Scherthan H

Subjects
Animals, Cell Cycle physiology, Cell Cycle Proteins genetics, Centromere metabolism, Humans, In Situ Hybridization, Fluorescence, Kinetochores metabolism, Meiosis physiology, RNA Interference, Rad51 Recombinase genetics, Rad51 Recombinase metabolism, Spindle Apparatus metabolism, Cell Cycle Proteins metabolism, Cell Line, Tumor physiology, Cell Line, Tumor radiation effects, Chromosome Segregation radiation effects, Gamma Rays, Neoplasms genetics, Neoplasms pathology, Polyploidy
Abstract

Escape from mitotic catastrophe and generation of endopolyploid tumour cells (ETCs) represents a potential survival strategy of tumour cells in response to genotoxic treatments. ETCs that resume the mitotic cell cycle have reduced ploidy and are often resistant to these treatments. In search for a mechanism for genome reduction, we previously observed that ETCs express meiotic proteins among which REC8 (a meiotic cohesin component) is of particular interest, since it favours reductional cell division in meiosis. In the present investigation, we induced endopolyploidy in p53-dysfunctional human tumour cell lines (Namalwa, WI-L2-NS, HeLa) by gamma irradiation, and analysed the sub-cellular localisation of REC8 in the resulting ETCs. We observed by RT-PCR and Western blot that REC8 is constitutively expressed in these tumour cells, along with SGOL1 and SGOL2, and that REC8 becomes modified after irradiation. REC8 localised to paired sister centromeres in ETCs, the former co-segregating to opposite poles. Furthermore, REC8 localised to the centrosome of interphase ETCs and to the astral poles in anaphase cells where it colocalised with the microtubule-associated protein NuMA. Altogether, our observations indicate that radiation-induced ETCs express features of meiotic cell divisions and that these may facilitate chromosome segregation and genome reduction.

Published
2009
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