The DOI matches its Crossref record, with a small difference in title or year; 43 of the 43 references it cites were found in a registry or an index.
BCR-ABL/GATA1/miR-138 mini circuitry contributes to the leukemogenesis of chronic myeloid leukemia
Abstract
Abnormal expression of microRNAs (miRNAs) has been implicated in carcinogenesis. Here we report a novel BCR (breakpoint cluster region)-ABL (c-abl oncogene 1, non-receptor tyrosine kinase)/GATA1/microRNA-138 (miR-138) circuitry in chronic myeloid leukemia (CML). miR-138 expression is downregulated in K562 cells and primary CML samples, which is restored after imatinib treatment. The tumor suppressor activity of miR-138 is demonstrated by the induction of cell cycle arrest at G0/G1, inhibition of cell proliferation and colony forming unit granulocyte-macrophage colony formation and enhanced imatinib-induced apoptosis in K562 and Ku812 cells overexpressing miR-138. Moreover, overexpression of miR-138 led to the downregulation of BCR-ABL. Based on luciferase assay, ABL and BCR-ABL are shown to be the target genes regulated by miR-138. Furthermore, miR-138 binding to ABL was shown to localize to the coding region instead of 3'-untranslated regions (3'-UTR) of ABL mRNA. In addition, CCND3 is another target of miR-138, which represses CCND3 expression by binding to its 3'-UTR. Finally, upregulation of miR-138 upon imatinib treatment is associated with the enhancement of GATA1 activity, which binds to the miR-138 promoter. In conclusion, miR-138 is a tumor suppressor miRNA underexpressed in CML. miR-138 represses expression of both BCR-ABL and CCND3 via binding to the coding region and 3'-UTR, respectively. miR-138 expression is activated by GATA1, which in turn is repressed by BCR-…
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“Moreover, neuronal downregulation of miR-138-5p may also induce cell death indirectly due to the overexpression of its proliferative and cell cycle targets including EZH2, E2F2, E2F3, CDK6, CCND3, or ABL1 [87,88,89].”
From MicroRNA-138-5p Targets Pro-Apoptotic Factors and Favors Neural Cell Survival: Analysis in the Injured Spinal Cord (2022) · cites this paper as [87]
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Cites
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Cited by
Hyaluronan abrogates imatinib-induced senescence in chronic myeloid leukemia cell lines
Lompardía, S., Díaz, M., Pibuel, M., Papademetrio, D., Poodts, D., Mihalez, C., Álvarez, É., & Hajos, S. (2019) · Scientific Reports · doi:10.1038/s41598-019-47248-8 · Cited by 19
Maza, R. M., Barreda-Manso, M. A., Reigada, D., Silván, Á., Muñoz-Galdeano, T., Soto, A., del Águila, Á., & Nieto-Díaz, M. (2022) · Biomedicines · doi:10.3390/biomedicines10071559 · Cited by 12
Metadata
- Authors
- Xu, C., Fu, H., Gao, L., Wang, L., Wang, W., Li, J., Li, Y., Dou, L., Gao, X., Luo, X., Jing, Y., Chim, C.-S., Zheng, X., & Yu, L.
- Venue
- Oncogene
- Published
- 2012-12-03
- Volume
- 33
- Issue
- 1
- Pages
- 44-54
- ISSN
- 0950-9232
- 1476-5594
- Cited by
- 58
- References
- 43
- Language
- en
- Licence
- www.springer.com/tdm (tdm)
- www.springer.com/tdm (vor)
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- Xu, C., Fu, H., Gao, L., Wang, L., Wang, W., Li, J., Li, Y., Dou, L., Gao, X., Luo, X., Jing, Y., Chim, C.-S., Zheng, X., & Yu, L. (2014). BCR-ABL/GATA1/miR-138 mini circuitry contributes to the leukemogenesis of chronic myeloid leukemia. Oncogene. https://doi.org/10.1038/onc.2012.557
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