miRNA-451: A putative predictor marker of Imatinib therapy response in chronic myeloid leukemia

Scholl, Vanesa; Hassan, Rocı́o; Zalcberg, Ilana

doi:10.1016/j.leukres.2011.08.023

Cited by 44 publications

(25 citation statements)

References 3 publications

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“…Recently, in a study with a small cohort of patients ( n = 17), it was suggested that the miR - 451 expression level found in total leukocytes of PB at diagnosis may be associated with the response to IM therapy. In addition, it was shown that the miR-451 level may inversely correlate with the BCR-ABL transcript level in some CML patients [56]. However, expression of miR-451 appears in this study to be relatively more heterogeneous.…”

Section: Micrornas In CMLmentioning

confidence: 56%

“…However, expression of miR-451 appears in this study to be relatively more heterogeneous. It was suggested that besides BCR-ABL, other mediators may be involved in the regulation of miR-451 expression [56]. Such heterogeneous expression of miR-451 expression among total leukocytes from CML patients may be explained by our unpublished data on the MNC and PMNC fractions from peripheral blood of six CML patients at diagnosis and after a short imatinib treatment (5–7 months).…”

Section: Micrornas In CMLmentioning

confidence: 95%

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Role of Epigenetics in Chronic Myeloid Leukemia

Poláková

Koblihova

Stopka

2013

Curr Hematol Malig Rep

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The efficacy of therapeutic modalities in chronic myeloid leukemia (CML) depends on both genetic and epigenetic mechanisms. This review focuses on epigenetic mechanisms involved in the pathogenesis of CML and in resistance of tumor cells to tyrosine kinase inhibitors leading to the leukemic clone escape and propagation. Regulatory events at the levels of gene regulation by transcription factors and microRNAs are discussed in the context of CML pathogenesis and therapeutic modalities.

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Section: Micrornas In CMLmentioning

confidence: 56%

Section: Micrornas In CMLmentioning

confidence: 95%

Role of Epigenetics in Chronic Myeloid Leukemia

Poláková

Koblihova

Stopka

2013

Curr Hematol Malig Rep

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“…miR-203 is silenced by genetic and epigenetic mechanisms in hematopoietic malignancies expressing either Abl1 or Bcr-Abl1, and restoration of miR-203 expression reduced Abl1 and Bcr-Abl1 levels and inhibited cell proliferation [32], [33]. In a recent study, miR-451 has also been shown to negatively regulate Bcr-Abl expression in chronic myeloid leukemia [34], [35]. However, such studies are lacking in prostate cancer.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-4723 Inhibits Prostate Cancer Growth through Inactivation of the Abelson Family of Nonreceptor Protein Tyrosine Kinases

et al. 2013

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The Abelson (c-Abl) proto-oncogene encodes a highly conserved nonreceptor protein tyrosine kinase that plays a role in cell proliferation, differentiation, apoptosis and cell adhesion. c-Abl represents a specific anti-cancer target in prostate cancer as aberrant activity of this kinase has been implicated in the stimulation of prostate cancer growth and progression. However, the mechanism of regulation of c-Abl is not known. Here we report that Abl kinases are regulated by a novel microRNA, miR-4723, in prostate cancer. Expression profiling of miR-4723 expression in a cohort of prostate cancer clinical specimens showed that miR-4723 expression is widely attenuated in prostate cancer. Low miR-4723 expression was significantly correlated with poor survival outcome and our analyses suggest that miR-4723 has significant potential as a disease biomarker for diagnosis and prognosis in prostate cancer. To evaluate the functional significance of decreased miR-4723 expression in prostate cancer, miR-4723 was overexpressed in prostate cancer cell lines followed by functional assays. miR-4723 overexpression led to significant decreases in cell growth, clonability, invasion and migration. Importantly, miR-4723 expression led to dramatic induction of apoptosis in prostate cancer cell lines suggesting that miR-4723 is a pro-apoptotic miRNA regulating prostate carcinogenesis. Analysis of putative miR-4723 targets showed that miR-4723 targets integrin alpha 3 and Methyl CpG binding protein in addition to Abl1 and Abl2 kinases. Further, we found that the expression of Abl kinase is inversely correlated with miR-4723 expression in prostate cancer clinical specimens. Also, Abl1 knockdown partially phenocopies miR-4723 reexpression in prostate cancer cells suggesting that Abl is a functionally relevant target of miR-4723 in prostate cancer. In conclusion, we have identified a novel microRNA that mediates regulation of Abl kinases in prostate cancer. This study suggests that miR-4723 may be an attractive target for therapeutic intervention in prostate cancer.

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“…Besides, miR-224 expression correlated with AML subtypes, in particular the t(15,17) rearrangement, a molecular predictor of favorable clinical outcome [151]. There were additional miRNAs implicated as chemoresistance biomarkers reported in hematological malignancies [152][153][154][155][156][157][158][159][160][161][162].…”

Section: Translating Mirnas Into Clinical Applications In Hematologicmentioning

confidence: 99%

Drug resistance-related microRNAs in hematological malignancies: Translating basic evidence into therapeutic strategies

Xie

Jing

et al. 2015

Blood Reviews

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miRNA-451: A putative predictor marker of Imatinib therapy response in chronic myeloid leukemia

Cited by 44 publications

References 3 publications

Role of Epigenetics in Chronic Myeloid Leukemia

Role of Epigenetics in Chronic Myeloid Leukemia

MicroRNA-4723 Inhibits Prostate Cancer Growth through Inactivation of the Abelson Family of Nonreceptor Protein Tyrosine Kinases

Drug resistance-related microRNAs in hematological malignancies: Translating basic evidence into therapeutic strategies

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