Functional validation of miRNAs targeting genes of DNA double-strand break repair to radiosensitize non-small lung cancer cells

Piotto, Celeste; Biscontin, Alberto; Millino, Caterina; Mognato, Maddalena

doi:10.1016/j.bbagrm.2018.10.010

Cited by 25 publications

(24 citation statements)

References 73 publications

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“…Upregulation of miR-101 sensitized glioblastoma and non-small cell lung cancer cell lines to IR (87). Another study demonstrated that transfection with has-miR-96-5p and has-miR-874-3p combined with IR decreased survival of non-small cell lung cancer cell lines when compared to IR alone, and had a similar effect when compared to a DNA-PK inhibitor (NU7026) plus IR (88).…”

Section: Pharmacotherapies Targeting Dna-pkmentioning

confidence: 99%

DNA-PK as an Emerging Therapeutic Target in Cancer

2019

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The DNA-dependent protein kinase (DNA-PK) plays an instrumental role in the overall survival and proliferation of cells. As a member of the phosphatidylinositol 3-kinase-related kinase (PIKK) family, DNA-PK is best known as a mediator of the cellular response to DNA damage. In this context, DNA-PK has emerged as an intriguing therapeutic target in the treatment of a variety of cancers, especially when used in conjunction with genotoxic chemotherapy or ionizing radiation. Beyond the DNA damage response, DNA-PK activity is necessary for multiple cellular functions, including the regulation of transcription, progression of the cell cycle, and in the maintenance of telomeres. Here, we review what is currently known about DNA-PK regarding its structure and established roles in DNA repair. We also discuss its lesser-known functions, the pharmacotherapies inhibiting its function in DNA repair, and its potential as a therapeutic target in a broader context.

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Section: Pharmacotherapies Targeting Dna-pkmentioning

confidence: 99%

DNA-PK as an Emerging Therapeutic Target in Cancer

2019

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“…Oncomir miR-34a negatively regulates the process of recombinant repair in NSCLC cells by binding to the 3 -untranslated region of RAD51 [114]. RAD51 expression was also significantly reduced in cells overexpressing hsa-miR-96-5p [115].…”

Section: Micrornas and Dna Repair In Lung Cancermentioning

confidence: 97%

Role of microRNAs in Lung Carcinogenesis Induced by Asbestos

Bersimbaev

Bulgakova

Aripova

et al. 2021

JPM

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MicroRNAs are a class of small noncoding endogenous RNAs 19–25 nucleotides long, which play an important role in the post-transcriptional regulation of gene expression by targeting mRNA targets with subsequent repression of translation. MicroRNAs are involved in the pathogenesis of numerous diseases, including cancer. Lung cancer is the leading cause of cancer death in the world. Lung cancer is usually associated with tobacco smoking. However, about 25% of lung cancer cases occur in people who have never smoked. According to the International Agency for Research on Cancer, asbestos has been classified as one of the cancerogenic factors for lung cancer. The mechanism of malignant transformation under the influence of asbestos is associated with the genotoxic effect of reactive oxygen species, which initiate the processes of DNA damage in the cell. However, epigenetic mechanisms such as changes in the microRNA expression profile may also be implicated in the pathogenesis of asbestos-induced lung cancer. Numerous studies have shown that microRNAs can serve as a biomarker of the effects of various adverse environmental factors on the human body. This review examines the role of microRNAs, the expression profile of which changes upon exposure to asbestos, in key processes of carcinogenesis, such as proliferation, cell survival, metastasis, neo-angiogenesis, and immune response avoidance.

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“…Other (PI3K)-like protein kinases that participate in cellular responses to DNA damage and coordinate H2AX phosphorylation can be regulated by miRNAs as well. For example, increased expression of miR-185 makes renal cell carcinoma cells more vulnerable to radiation by regulating ATR expression at the post-transcriptional level [88], miR-874-3p targets DNA-PKcs, which also recruits and activates the downstream components in the NHEJ pathway of DSB repair [89] and miR-101 binds to both DNA-PKcs and ATM mRNAs and regulates them post-transcriptionally in various human cell lines (Figure 2) [90].…”

Section: Rna Regulating the Recognition Of Dsbmentioning

confidence: 99%

The Role of RNA in DNA Breaks, Repair and Chromosomal Rearrangements

et al. 2021

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Incorrect reparation of DNA double-strand breaks (DSB) leading to chromosomal rearrangements is one of oncogenesis’s primary causes. Recently published data elucidate the key role of various types of RNA in DSB formation, recognition and repair. With growing interest in RNA biology, increasing RNAs are classified as crucial at the different stages of the main pathways of DSB repair in eukaryotic cells: nonhomologous end joining (NHEJ) and homology-directed repair (HDR). Gene mutations or variation in expression levels of such RNAs can lead to local DNA repair defects, increasing the chromosome aberration frequency. Moreover, it was demonstrated that some RNAs could stimulate long-range chromosomal rearrangements. In this review, we discuss recent evidence demonstrating the role of various RNAs in DSB formation and repair. We also consider how RNA may mediate certain chromosomal rearrangements in a sequence-specific manner.

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Functional validation of miRNAs targeting genes of DNA double-strand break repair to radiosensitize non-small lung cancer cells

Cited by 25 publications

References 73 publications

DNA-PK as an Emerging Therapeutic Target in Cancer

DNA-PK as an Emerging Therapeutic Target in Cancer

Role of microRNAs in Lung Carcinogenesis Induced by Asbestos

The Role of RNA in DNA Breaks, Repair and Chromosomal Rearrangements

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