The DNA-Damage Response to γ-Radiation Is Affected by  miR-27a in A549 Cells

Francesco, Andrea Di; Pittà, Cristiano De; Moret, Francesca; Barbieri, Vito; Celotti, Lucia; Mognato, Maddalena

doi:10.3390/ijms140917881

Cited by 34 publications

(20 citation statements)

References 47 publications

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“…For example, ATM has been shown to be a gene target of a variety of miRNAs, including miR-223, miR-181a, miR26a, miR-27a, miR-214, and miR-18a [61][62][63][64][65][66][67]. These miRNAs enhance sensitivity to IR and etoposide by regulating the ATMmediated signaling pathway.…”

Section: Mirnas Regulate Ddr Transducersmentioning

confidence: 97%

Non-coding RNAs: An emerging player in DNA damage response

Zhang

Peng

2015

Mutation Research/Reviews in Mutation Research

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Section: Mirnas Regulate Ddr Transducersmentioning

confidence: 97%

Non-coding RNAs: An emerging player in DNA damage response

Zhang

Peng

2015

Mutation Research/Reviews in Mutation Research

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“…In addition, aberrant expression of miRNAs has been implicated in various aspects of cancer biology by regulating cancer cell survival, apoptosis, invasion and metastasis . With regard to the response of cancer cells to ionizing radiation (IR), an increasing number of IR‐responsive miRNAs and miRNAs that modulate cancer cell responses to IR have been identified .…”

Section: Introductionmentioning

confidence: 99%

Ionizing radiation‐inducible miR‐30e promotes glioma cell invasion through EGFR stabilization by directly targeting CBL‐B

et al. 2015

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MicroRNAs (miRNAs) are small non-coding RNA molecules that regulate gene expression at the transcriptional and post-transcriptional levels. Here we show that miR-30e, which was previously identified as an ionizing radiation-inducible miRNA, enhances cellular invasion by promoting secretion of the matrix metalloproteinase MMP-2. The enhancement of cellular invasion by miR-30e involved up-regulation of the epidermal growth factor receptor (EGFR) and subsequent activation of its downstream signaling mediators, AKT and extracellular signal-regulated kinase. EGFR up-regulation by miR-30e occurred due to stabilization of the EGFR protein. The E3 ubiquitin ligase casitas B-lineage lymphoma B (CBL-B) was down-regulated by miR-30e, and this led to increased EGFR abundance. A 3 0 UTR reporter assay confirmed that CBL-B is a direct target of miR-30e. Knocking down CBL-B expression phenocopied the effects of miR-30e, whereas ectopic expression of CBL-B suppressed miR-30e-induced EGFR up-regulation and invasion. Collectively, our results suggest that targeting miR-30e may limit the invasiveness induced during glioma radiotherapy.

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“…for reviews of the relationship between miRNA expression and radioresponse. These changes often occur through alterations in: the expression of key DDR proteins; cell cycle regulatory proteins; regulation of cellular radical oxygen species; and proliferation of apoptosis genes such as p53, ATM, ATR, NFKB, and BCL2.…”

Section: Transcript Level Analysis (Noncoding Rna Transcripts)mentioning

confidence: 99%

Radiogenomics

Story

Durante

2018

Medical Physics

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Purpose Radiogenomics is the study of genomic changes that underlie the radioresponse of normal and tumor tissues. And while this is generally regarded as a whole genome approach, one must keep in mind the impact of single gene biology on radioresponse, (ataxia telangiectasia, Nijmegen breakage syndrome). Methods This review begins with the association of single nucleotide polymorphisms in the DNA with adverse normal tissue events to the prediction of therapeutic outcome after radiotherapy. From there it covers transcriptome (protein coding RNA transcripts) analysis, which is where the greatest understanding of the molecular signaling responsible for the radioresponse of tumors and normal tissues is known. Non‐protein coding RNA transcripts (miRNA, lncRNA), transcribed from what was once thought of as junk DNA, are now known to be negative regulators of the transcription of mRNA by multiple mechanisms. miRNA can act as tumor suppressors or oncogenes regulating a diverse range of cellular processes that drive radioresponse and biosignatures that predict outcome after radiotherapy are described. Results Biological signatures that explain differences in radioresponse based upon cell type, biological signatures that predict surviving fraction at 2 Gy and signatures that identify hypoxia have been described. The omics analysis of the response of mammalian cells to charged particle, predominantly proton and carbon ions, is less mature than that seen with low LET radiation exposures. However, there appear to be responses after charged particle exposure that parallel the responses seem with low LET exposures. This commonality of response is centered around the downstream signaling of p53. There are also novel omics responses to charged particles that help explain the response of tumors to charged particle exposures. For instance, signaling pathways associated with angiogenesis, vasculogenesis, migration and invasion appear to be downregulated in a number of cell types when exposed to charged particles. This response supports both in vitro and in vivo data suggesting that tumors exposed to charged particles are less invasive, unlike the response of tumors to low LET exposures. Profoundly lacking for low LET and charged particle exposures are predictive or prognostic signatures of radioresponse or tumor physiology affecting radioresponse that have been validated in prospective clinical trials. For example, the identification of low LET tumor radioresistance could be used as a marker of patient eligibility for carbon therapy. Tissue specific signatures, or accurate imaging of hypoxic regions, could be used for charged particle selection to overcome hypoxia per se, or could be used to prescribe a high LET therapeutic boost to a hypoxic region of a tumor. Conclusions Integrating radiogenomics into radiation oncology has the potential to personalize an already precise form of cancer therapy.

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The DNA-Damage Response to γ-Radiation Is Affected by miR-27a in A549 Cells

Cited by 34 publications

References 47 publications

Non-coding RNAs: An emerging player in DNA damage response

Non-coding RNAs: An emerging player in DNA damage response

Ionizing radiation‐inducible miR‐30e promotes glioma cell invasion through EGFR stabilization by directly targeting CBL‐B

Radiogenomics

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