Synergistic apoptosis induction in leukemic cells by miR-15a/16-1 and arsenic trioxide

Gao, Shenmeng; Chen, Chiqi; Wu, Jianbo; Tan, Yue; Kang, Yu; Xing, Chongyun; Ye, Aifang; Liang, Yin; Jiang, Lei

doi:10.1016/j.bbrc.2010.10.137

Cited by 30 publications

(21 citation statements)

References 32 publications

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“…In present study, we first explored the potential effects on occupational benzene exposure and CBP on plasma miRNA expression in Chinese occupational population. Previous studies have demonstrated that the alteration of miRNAs expression played important roles in cell transformation, particularly in the process of chemical carcinogenesis (32)(33)(34). Our microarray analysis and subsequent validation identified four indicated miRNAs in plasma that may affect the responses to benzene exposure, which may also provide a new perspective on the pathogenesis of CBP.…”

Section: Discussionmentioning

confidence: 62%

Analysis of plasma microRNA expression profiles in a Chinese population occupationally exposed to benzene and in a population with chronic benzene poisoning

Liu¹,

Chen

Bian

et al. 2016

J. Thorac. Dis.

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Background: Circulating microRNA (miRNA) has attractive interests as a non-invasive biomarker of physiological and pathological conditions. Our study aimed to investigate the potential effects of chronic benzene poisoning (CBP) and benzene exposure on miRNA expression, and identify CBP-related miRNAs. Methods:In the discovery stage, we used a microarray assay to detect the miRNA expression profiles among pooled plasma samples from ten CBP patients, ten healthy benzene-exposed individuals and ten nonbenzene exposed individuals. Subsequently, we conducted an expanded validation of six candidate miRNAs in 27 CBP patients-low blood counts, 54 healthy benzene-exposed individuals and 54 non-exposed individuals.Moreover, we predicted the biological functions of putative target genes using a Gene Ontology (GO) function enrichment analysis and KEGG pathway analysis.Results: In the discovery stage, compared with non-exposures, 36 and 12 miRNAs demonstrated at least a 1.0-fold differential expression in the CBP patients and the benzene exposures, respectively. And compared with benzene exposures, 58 miRNAs demonstrated at least a 1.0-fold differential expression in the CBP patients. In the expanded validation stage, compared with non-exposures as well as exposures, miR-24-3p and miR-221-3p were significantly up-regulated (1.99-and 2.06-fold for miR-24-3p, 2.19-and 3.93-fold for miR-221-3p, P<0.01) while miR-122-5p and miR-638 were significantly down-regulated (−3.45-and −2.60-fold for miR-122-5p, −1.82-and −3.20-fold for miR-638, P<0.001) in the CBP patients; compared with non-exposures, the plasma level of miR-638 was significantly up-regulated (1.38-fold, P<0.01) while the plasma levels miR-122-5p and miR-221-3p were significantly down-regulated (−0.85-and −1.74-fold, P<0.01) in the exposures, which were consistent with the results of microarray analysis. Conclusions:The four indicated plasma miRNAs may be biomarkers of indicating responses to benzene exposure. Further studies are warranted to verify our findings with a large sample and to confirm the underlying mechanisms.

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Section: Discussionmentioning

confidence: 62%

Analysis of plasma microRNA expression profiles in a Chinese population occupationally exposed to benzene and in a population with chronic benzene poisoning

Liu¹,

Chen

Bian

et al. 2016

J. Thorac. Dis.

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“…One of the first studies to link miRNA-mediated mitochondrial dysfunction with cancer showed that mir-15a induces an efflux of cytochrome c and disrupts the mitochondrial membrane potential [116]. In CLL, mir-15a is frequently deleted [48].…”

Section: Disparities At the Nuclear Genome Level And Their Role Inmentioning

confidence: 99%

“…The same study also reported a putative mitochondrial localization sequence in HER1. A later study showed that the mitochondrial uptake of HER1 was increased upon exposure to apoptosis inducers and that, in cancer cells, mitochondrial targeting of HER1 was responsible for drug resistance [115, 116]. Together, these findings indicate that mitochondrial HER is involved in modulating metabolism, apoptosis, and cell survival.…”

Section: Disparities At the Nuclear Genome Level And Their Role Inmentioning

confidence: 99%

Mitochondrial determinants of cancer health disparities

Choudhury

Singh

2017

Seminars in Cancer Biology

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Mitochondria are involved in the generation of energy, cell growth and differentiation, cellular signaling, cell cycle control, and cell death. To date, the mitochondrial basis of cancer disparities is unknown. The goal of this review is to provide an understanding and a framework of mitochondrial determinants that may contribute to cancer disparities in racially different populations. Mitochondria, which are multi-functional, have been implicated in the initiation and progression of cancers in relation to metabolic alterations in transformed cells. Due to ethnic-based diversity, the mitochondrial genome (mtDNA) could be a basis for inherited racial disparities and for acquired somatic mutations during tumorigenesis. In African Americans, several germline, population-specific haplotype variants in mtDNA as well as depletion of mtDNA have been linked to cancer predisposition and cancer disparities. Indeed, depletion of mtDNA and mutations in mtDNA or nuclear genome (nDNA)-encoded mitochondrial proteins lead to mitochondrial dysfunction and promote resistance to apoptosis, the epithelial-to-mesenchymal transition, and metastatic disease, which in turn can contribute to cancer disparity and tumor aggressiveness related to racial disparities. Ethnic differences at the level of expression or genetic variations in nDNA encoding the mitochondrial proteome, including mitochondria-localized mtDNA replication and repair proteins, miRNA, transcription factors, kinases and phosphatases, and tumor suppressors and oncogenes may underlie susceptibility to high-risk and aggressive cancers found in African Americans and other ethnicities. The mitochondrial retrograde signaling that alters the expression profile of nuclear genes in response to dysfunctional mitochondria is a mechanism for tumorigenesis. In ethnic populations, differences in mitochondrial function may alter the cross talk between mitochondria and the nucleus at epigenetic and genetic levels, which can also contribute to cancer health disparities. Targeting mitochondrial determinants and mitochondrial retrograde signaling could provide a promising strategy for the development of selective anticancer therapy for dealing with cancer disparities. Further, agents that restore mitochondrial function to optimal levels should permit sensitivity to anticancer agents for the treatment of aggressive tumors that occur in racially diverse populations and hence help in reducing racial disparities.

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“…Furthermore, MiR-15a promotes mitochondrial dysfunction resulting in cytochrome c release into the cytoplasm and the dissipation of the mitochondrial membrane potential (ΔΨ m,i ) (Gao et al 2010 ). MiR-210, MiR-181, and the muscle-specifi c MiR-1 have been reported to be increased upon apoptotic stimulation and found to be associated with the release of cytochrome c from mitochondria and the ΔΨ m,i decrease (Chio et al 2013 ;Ouyang et al 2012 ;Yu et al 2008 ).…”

Section: Micrornas and Mitochondria-induced Cell Deathmentioning

confidence: 99%