LINE-1 Retrotransposons and Their Role in Cancer

Rahbari, Raheleh; Habibi, Laleh; García-Puche, José L.; Badge, Richard M.; García‐Pérez, José L.

doi:10.1007/978-94-017-9639-2_3

Cited by 2 publications

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“…Class I mobile elements use RNA intermediate and reverse transcriptase activity for transposition, while Class II elements use a DNA intermediate and a ‘cut and paste’ mechanism. Class I elements include long terminal repeat (LTR) retrotransposons, also called ‘endogenous retroviruses’ (ERVs), and non-long terminal repeat (non-LTR) retrotransposons (LINEs and SINEs) [ 155 ]. Human transposable elements comprise about 40 % of the human genome: HERVs, 4.64 %; MaLR, 3.65 %; LINEs, 20.42 %; and SINEs, 13.14 % [ 100 ].…”

Section: Introductionmentioning

confidence: 99%

“…The younger retroelements are highly methylated in healthy tissues, while in many tumors these young elements suffer the most dramatic loss of methylation [ 49 , 130 , 186 ]. L1 and Alu sequences are silenced in normal human cells and activated in tumors [ 14 , 155 , 171 ]. Full length L1 RNA in cancer cell lines and expression of ORF1p in tumors have been shown (reviewed in [ 130 ]).…”

Section: Introductionmentioning

confidence: 99%

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Expression of evolutionarily novel genes in tumors

Kozlov

2016

Infect Agents Cancer

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The evolutionarily novel genes originated through different molecular mechanisms are expressed in tumors. Sometimes the expression of evolutionarily novel genes in tumors is highly specific. Moreover positive selection of many human tumor-related genes in primate lineage suggests their involvement in the origin of new functions beneficial to organisms.It is suggested to consider the expression of evolutionarily young or novel genes in tumors as a new biological phenomenon, a phenomenon of TSEEN (tumor specifically expressed, evolutionarily novel) genes.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Expression of evolutionarily novel genes in tumors

Kozlov

2016

Infect Agents Cancer

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MicroRNA-34a Encapsulated in Hyaluronic Acid Nanoparticles Induces Epigenetic Changes with Altered Mitochondrial Bioenergetics and Apoptosis in Non-Small-Cell Lung Cancer Cells

Trivedi

Singh

Talekar

et al. 2017

Sci Rep

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Therapies targeting epigenetic changes for cancer treatment are in Phase I/II trials; however, all of these target only nuclear DNA. Emerging evidence suggests presence of methylation marks on mitochondrial DNA (mtDNA); but their contribution in cancer is unidentified. Expression of genes encoded on mtDNA are altered in cancer cells, along with increased glycolytic flux. Such glycolytic flux and elevated reactive oxygen species is supported by increased antioxidant; glutathione. MicroRNA-34a can translocate to mitochondria, mediate downstream apoptotic effects of tumor suppressor P53, and inhibit the antioxidant response element Nrf-2, resulting in depleted glutathione levels. Based on such strong rationale, we encapsulated microRNA-34a in our well-established Hyaluronic-Acid nanoparticles and delivered to cisplatin-sensitive and cisplatin-resistant A549-lung adenocarcinoma cells. Successful delivery and uptake in cells resulted in altered ATP levels, decreased glycolytic flux, Nrf-2 and glutathione levels, ultimately resulting in caspase-3 activation and apoptosis. Most important were the concurrent underlying molecular changes in epigenetic status of D-loop on the mtDNA and transcription of mtDNA-encoded genes. Although preliminary, we provide a novel therapeutic approach in form of altered mitochondrial bioenergetics and redox status of cancer cells with underlying changes in epigenetic status of mtDNA that can subsequently results in induction of cancer cell apoptosis.

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LINE-1 Retrotransposons and Their Role in Cancer

Cited by 2 publications

References 222 publications

Expression of evolutionarily novel genes in tumors

Expression of evolutionarily novel genes in tumors

MicroRNA-34a Encapsulated in Hyaluronic Acid Nanoparticles Induces Epigenetic Changes with Altered Mitochondrial Bioenergetics and Apoptosis in Non-Small-Cell Lung Cancer Cells

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