We are analyzing https://link.springer.com/article/10.1186/1475-2867-6-13.

Title:
Human LINE-1 retrotransposon induces DNA damage and apoptosis in cancer cells | Cancer Cell International
Description:
Background Long interspersed nuclear elements (LINEs), Alu and endogenous retroviruses (ERVs) make up some 45% of human DNA. LINE-1 also called L1, is the most common family of non-LTR retrotransposons in the human genome and comprises about 17% of the genome. L1 elements require the integration into chromosomal target sites using L1-encoded endonuclease which creates staggering DNA breaks allowing the newly transposed L1 copies to integrate into the genome. L1 expression and retrotransposition in cancer cells might cause transcriptional deregulation, insertional mutations, DNA breaks, and an increased frequency of recombinations, contributing to genome instability. There is however little evidence on the mechanism of L1-induced genetic instability and its impact on cancer cell growth and proliferation. Results We report that L1 has genome-destabilizing effects indicated by an accumulation of γ-H2AX foci, an early response to DNA strand breaks, in association with an abnormal cell cycle progression through a G2/M accumulation and an induction of apoptosis in breast cancer cells. In addition, we found that adjuvant L1 activation may lead to supra-additive killing when combined with radiation by enhancing the radiation lethality through induction of apoptosis that we have detected through Bax activation. Conclusion L1 retrotransposition is sensed as a DNA damaging event through the creation DNA breaks involving L1-encoded endonuclease. The apparent synergistic interaction between L1 activation and radiation can further be utilized for targeted induction of cancer cell death. Thus, the role of retrotransoposons in general, and of L1 in particular, in DNA damage and repair assumes larger significance both for the understanding of mutagenicity and, potentially, for the control of cell proliferation and apoptosis.
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Keywords {🔍}

cells, dna, cell, retrotransposition, rcl, article, pubmed, google, scholar, cas, expression, human, apoptosis, damage, cancer, orf, breaks, genome, repair, γhax, cycle, mcf, transfected, polyclonal, integration, antibody, response, figure, induction, antil, hax, line, endonuclease, genomic, rabbit, foci, assay, central, authors, analysis, egfp, performed, dsbs, elements, activation, radiation, control, expressing, antibodies, retroviral,

Topics {✒️}

anti-γ-tubulin mouse monoclonal anti-γ-h2ax rabbit polyclonal dna double-strand breaks anti-γ-h2ax polyclonal antibody single-strand breaks introduced rc-l1-expressing cells passaged rc-l1-expressing cells determined anti-bax polyclonal antibody rc-l1-egfp-expressing cells rc-l1-expressing mcf-7 cells fitc-conjugated secondary antibody open access article mcf-7 cells-expressing l1-egfp double-strand breaks hrp-conjugated secondary antibodies anti-l1 orf2 antibody human rc-l1 tagged article download pdf human line-1 retrotransposon dna strand breaks pro-apoptotic gene anti-l1 orf2 antibodies anti-l1-orf2 antibodies tagged rc-l1 clones rc-l1- expression determined full size image concerted cleavage-ligation reaction rc-l1 expressing cells rc-l1-expressing cells assaying rc-l1 expression cellular dna damage-response l1-egfp plasmid showing wild-type orf2 expression providing l1-egfp construct γ-h2ax foci formation dna-pk function redundantly γ-h2ax foci assay l1-induced genetic instability target-primed reverse transcription long terminal repeats results rc-l1 expression anti-bax antibody dna damage-induced apoptosis rc-l1 transfected cells single strand links dna repair pathways dmem complete medium anti-α-tubulin anti-orf2 antibody l1-encoded endonuclease

Schema {🗺️}

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         description:Long interspersed nuclear elements (LINEs), Alu and endogenous retroviruses (ERVs) make up some 45% of human DNA. LINE-1 also called L1, is the most common family of non-LTR retrotransposons in the human genome and comprises about 17% of the genome. L1 elements require the integration into chromosomal target sites using L1-encoded endonuclease which creates staggering DNA breaks allowing the newly transposed L1 copies to integrate into the genome. L1 expression and retrotransposition in cancer cells might cause transcriptional deregulation, insertional mutations, DNA breaks, and an increased frequency of recombinations, contributing to genome instability. There is however little evidence on the mechanism of L1-induced genetic instability and its impact on cancer cell growth and proliferation. We report that L1 has genome-destabilizing effects indicated by an accumulation of γ-H2AX foci, an early response to DNA strand breaks, in association with an abnormal cell cycle progression through a G2/M accumulation and an induction of apoptosis in breast cancer cells. In addition, we found that adjuvant L1 activation may lead to supra-additive killing when combined with radiation by enhancing the radiation lethality through induction of apoptosis that we have detected through Bax activation. L1 retrotransposition is sensed as a DNA damaging event through the creation DNA breaks involving L1-encoded endonuclease. The apparent synergistic interaction between L1 activation and radiation can further be utilized for targeted induction of cancer cell death. Thus, the role of retrotransoposons in general, and of L1 in particular, in DNA damage and repair assumes larger significance both for the understanding of mutagenicity and, potentially, for the control of cell proliferation and apoptosis.
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      headline:Human LINE-1 retrotransposon induces DNA damage and apoptosis in cancer cells
      description:Long interspersed nuclear elements (LINEs), Alu and endogenous retroviruses (ERVs) make up some 45% of human DNA. LINE-1 also called L1, is the most common family of non-LTR retrotransposons in the human genome and comprises about 17% of the genome. L1 elements require the integration into chromosomal target sites using L1-encoded endonuclease which creates staggering DNA breaks allowing the newly transposed L1 copies to integrate into the genome. L1 expression and retrotransposition in cancer cells might cause transcriptional deregulation, insertional mutations, DNA breaks, and an increased frequency of recombinations, contributing to genome instability. There is however little evidence on the mechanism of L1-induced genetic instability and its impact on cancer cell growth and proliferation. We report that L1 has genome-destabilizing effects indicated by an accumulation of γ-H2AX foci, an early response to DNA strand breaks, in association with an abnormal cell cycle progression through a G2/M accumulation and an induction of apoptosis in breast cancer cells. In addition, we found that adjuvant L1 activation may lead to supra-additive killing when combined with radiation by enhancing the radiation lethality through induction of apoptosis that we have detected through Bax activation. L1 retrotransposition is sensed as a DNA damaging event through the creation DNA breaks involving L1-encoded endonuclease. The apparent synergistic interaction between L1 activation and radiation can further be utilized for targeted induction of cancer cell death. Thus, the role of retrotransoposons in general, and of L1 in particular, in DNA damage and repair assumes larger significance both for the understanding of mutagenicity and, potentially, for the control of cell proliferation and apoptosis.
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      affiliation:
            name:Cornell University
            address:
               name:Center for Reproductive Medicine and Infertility, Weill Medical College, Cornell University, New York, USA
               type:PostalAddress
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      affiliation:
            name:Eastern Virginia Medical School
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               name:Department of Microbiology and Molecular Cell Biology, Eastern Virginia Medical School, Norfolk, USA
               type:PostalAddress
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