**Author details**

*Advances in Hematologic Malignancies*

B-cell ALL [76].

expression levels in cancer, can represent a viable therapeutic strategy and a powerful intervention tool in **leukemia** [73]. For example, in leukemia cells isolated from individuals with BCR/ABL, TKI-resistant Philadelphia-chromosome-positive acute lymphoblastic leukemia (Ph + ALL) was observed an increase in levels of DNMT3A in association with downregulation of miR-217; these observations are clinically relevant; and inhibition of DNMT3A by forced expression of miRNA-217 may benefit in preventing drug resistance to TKI treatment in Philadelphiachromosome-positive ALL patients [74]. Another therapeutic strategy for

BCR-ABL-positive ALL is miRNA-203, which has as direct target to BCR-ABL1 and ABL1, proteins with activity tyrosine kinase. This miRNA is silenced by genetic and epigenetic mechanisms in hematopoietic malignancies expressing either ABL1 or BCR-ABL1. However, the restoration of the miRNA-203 expression reduces ABL1 and BCR-ABL1 levels and inhibits cell proliferation [75]. miRNA-143 was identified as a regulator of MLL-AF4 expression and is epigenetically repressed by promoter hypermethylation in MLL-AF4-positive primary blasts and cell lines;upregulation of miRNA-143 expression by demethylation has therapeutic promise for MLL-AF4

It is also important to consider that some miRNAs can behave as oncogenes in one cancer type and as tumor suppressive genes in others. It has been reported that miR-221 maintains a high expression in hepatic cancer and exerts an oncogenic function by targeting tumor suppressor PTEN, but this miRNA acts as a tumor suppressor in erythroblastic leukemia by inhibiting the KIT oncogene expression [77, 78]. Thus, identification of specific biological functions, type of cancer, and targets of miRNAs

Various studies have demonstrated that the oncomiRs or tumor suppressor miRNAs expression may significantly have potential how diagnostic and/ or prognostic biomarkers, as well as monitoring the disease progression and in the response to treatment, and it may be a therapeutic target for treatment in ALL. Also, miRNAs expression levels may play an important role in the genesis and evolution of the ALL. Nevertheless, the biological effects and relevant target genes of many miRNAs that are deregulated and/or prognostically relevant in ALL need to be identified and characterized. Therefore, novel anti-ALL agents are needed to overcome chemotherapy resistance and reduce cytotoxicity. The mimics- and/or anti-miRNAs may be a good alternative. However, more experiments are required to evaluate the feasibility and safety of mimics- and/or anti-miRNAs

This work was supported by the Universidad Autónoma de Guerrero. Yazmín Gómez-Gómez (CVU: 236728) and Jorge Organista-Nava (CVU: 236745) were

is a basic aspect when considering miRNA therapeutics.

recipient of postdoctoral fellowships from CONACYT.

The authors declare that there are no conflicts of interest.

**8. Summary and future directions**

in the clinical treatment.

**Acknowledgements**

**Conflict of interest**

**64**

Yazmín Gómez-Gómez† , Jorge Organista-Nava\*† , Berenice Illades-Aguiar and Marco Antonio Leyva-Vázquez\* Molecular Biomedicine Laboratory, School of Chemical-Biological Sciences, Autonomous University of Guerrero, Chilpancingo, Guerrero, Mexico

\*Address all correspondence to: leyvamarco13@gmail.com and joorna@gmail.com

† These authors contributed equally to this work

© 2019 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
