Protective role of miR-155 in breast cancer through
            <i>RAD51</i>
            targeting impairs homologous recombination after irradiation

Gasparini, Pierluigi; Lovat, Francesca; Fassan, Matteo; Casadei, Lucia; Cascione, Luciano; Jacob, Naduparambil K.; Carasi, Stefania; Palmieri, Dario; Costinean, Stefan; Shapiro, Charles L.; Huebner, Kay; Croce, Carlo M.

doi:10.1073/pnas.1402604111

Cited by 184 publications

(151 citation statements)

References 48 publications

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“…The present study observed that the phosphorylation levels of AKT and ERK representative of signaling pathway activation decreased subsequent to miR-155 silencing, but it has yet to be determined whether the mechanism involves the regulation of PTEN expression. However, it has been revealed that the role of miR-155 in tumors involves multiple aspects and miR-155 interacts with the intracellular transcription factors regulating gene transcription (42,43). The present results demonstrated the ability of miR-155 to positively regulate the activity of NF-κB and AP-1.…”

Section: A B C D E Fsupporting

confidence: 55%

Effect of miR-155 knockdown on the reversal of doxorubicin resistance in human lung cancer A549/dox cells

et al. 2015

Oncology Letters

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Abstract. Doxorubicin has been widely used in the treatment of cancer. However, acquired doxorubicin resistance severely hinders the application of the drug. In the present study, doxorubicin resistance was investigated in lung carcinoma. microRNA-155 (miR-155) was found to be upregulated in the doxorubicin-resistant A549/dox cell line. Suppression of miR-155 in this cell line considerably reversed doxorubicin resistance, and doxorubicin-induced apoptosis and cell cycle arrest were recovered. Furthermore, reverse transcription-polymerase chain reaction and western blot analysis revealed that miR-155 suppression downregulated the expression of multidrug resistance protein 1, multidrug resistance-associated protein 1, breast cancer resistance protein, glutathione S-transferase-π, Survivin and B-cell lymphoma 2, and upregulated the expression of caspase-3 and caspase-8. In addition, it was found that miR-155 suppression inhibited the activation of AKT and extracellular signal-regulated kinase. The transcriptional activity of nuclear factor-κB and activator protein-1 was also downregulated. In summary, the present results indicate that miR-155 may participate in doxorubicin resistance in lung carcinoma. The current study provides a novel target for lung carcinoma treatment.

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Section: A B C D E Fsupporting

confidence: 55%

Effect of miR-155 knockdown on the reversal of doxorubicin resistance in human lung cancer A549/dox cells

et al. 2015

Oncology Letters

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“…The cells were seeded onto a 6-well plate at a density of 3x10 5 /well overnight. The cells were then collected and HK activities were measured using the Hexokinase Colorimetric Assay kit (Sigma-Aldrich China, Inc.), according to the manufacturer's protocol.…”

Section: Ionizing Radiation Treatment Approximately 5x10mentioning

confidence: 99%

“…The cells were seeded onto a 6-well plate at a density of 3x10 5 /well, and the culture medium was replaced with low glucose DMEM (Invitrogen; Thermo Fisher Scientific, Inc.) after 6 h. The concentrations of glucose and L-lactate were measured after a further 24 h using a Glucose Test kit (Applygen Technologies, Inc., Beijing, China) and an L-lactate Assay kit (Eton Bioscience, Inc., San Diego, CA, USA), respectively, according to the manufacturer's instructions.…”

Section: Ionizing Radiation Treatment Approximately 5x10mentioning

confidence: 99%

“…Usually, miRNAs that lead to tumorigenesis are classed as oncomiRs, whereas miRNAs whose functional loss can contribute to the malignant transformation of normal cells, are classed as tumor suppressors (3). miRNA (miR)-155 is one of the most commonly upregulated miRNAs in several types of cancer, including non-small cell lung cancer (NSCLC) (4), breast cancer (5), pancreatic cancer (6), colon cancer (7), renal cancer (8), Hodgkin and B cell lymphoma (9), and secondary acute leukemia (10). Therefore, the dysregulated expression of miR-155 may be an important target for the diagnosis, prognosis and treatment of cancer (11).…”

Section: Introductionmentioning

confidence: 99%

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Inhibition of microRNA-155 sensitizes lung cancer cells to irradiation via suppression of HK2-modulated glucose metabolism

Zhang

et al. 2016

Molecular Medicine Reports

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Abstract. MicroRNAs (miRNAs) are small non-coding regulatory RNAs, which are involved in the post-transcriptional regulation of gene expression. miRNA (miR)-155, which has previously been reported to be overexpressed in lung cancer, is correlated with poor patient prognosis. The present study aimed to investigate the effects of miR-155 on the radiosensitivity of human non-small cell lung cancer (NSCLC) cells. To explore the roles of miRNAs in the regulation of irradiation sensitivity of human lung cancer cells, the expressions of miR-155 in response to irradiation, have been studied by RT-qPCR, and the putative direct target of miR-155 was identified by western blot and luciferase assays. The results of the present study revealed that the expression of miR-155 was induced by irradiation, thus suggesting a positive correlation between miR-155 and radiosensitivity. Furthermore, overexpression of miR-155 rendered lung cancer cells resistant to irradiation. In addition, hexokinase 2 (HK2) was identified as an indirect target of miR-155; exogenous overexpression of miR-155 upregulated the expression of HK2, whereas inhibition of miR-155 by antisense miRNA suppressed HK2 expression. In addition, HK2-modulated glucose metabolism was significantly upregulated by overexpression of miR-155. Notably, inhibition of miR-155 sensitized lung cancer cells to irradiation via suppression of glucose metabolism. In conclusion, the present study reported a novel function for miR-155 in the regulation of NSCLC cell radiosensitivity, thus suggesting that miR-155 may be considered a therapeutic target for the development of anticancer drugs.

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“…Studies have identified some novel miRNAs which are involved in the DNA repair pathway and regulate the DNA damage response to radiation (29)(30)(31). Yan et al (32) identified miR-101 as a molecule able to sensitize cancer cells to IR by targeting the 3'UTR of DNA-PKcs and ATM transcripts.…”

Section: Discussionmentioning

confidence: 99%

Knockdown of microRNA-1323 restores sensitivity to radiation by suppression of PRKDC activity in radiation-resistant lung cancer cells

Han

et al. 2015

Oncology Reports

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Abstract.Resistance to radiation is a major problem in cancer treatment. The mechanisms of radioresistance remain poorly understood; however, mounting evidence supports a role for microRNAs (miRNAs) in the modulation of key cellular pathways mediating the response to radiation. The present study aimed to identify specific miRNAs and their effect on radioresistant cells. The global miRNA profile of an established radioresistant lung cancer cell line and the corresponding control cells was determined.

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Protective role of miR-155 in breast cancer through RAD51 targeting impairs homologous recombination after irradiation

Cited by 184 publications

References 48 publications

Effect of miR-155 knockdown on the reversal of doxorubicin resistance in human lung cancer A549/dox cells

Effect of miR-155 knockdown on the reversal of doxorubicin resistance in human lung cancer A549/dox cells

Inhibition of microRNA-155 sensitizes lung cancer cells to irradiation via suppression of HK2-modulated glucose metabolism

Knockdown of microRNA-1323 restores sensitivity to radiation by suppression of PRKDC activity in radiation-resistant lung cancer cells

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