Exploring the role of GHRH antagonist MIA-602 in overcoming Doxorubicin-resistance in acute myeloid leukemia

Simonetta I. Gaumond; Rama Abdin; Joel Costoya; Andrew V. Schally; Joaquin J. Jimenez

doi:10.18632/oncotarget.28579

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Research Papers:

Exploring the role of GHRH antagonist MIA-602 in overcoming Doxorubicin-resistance in acute myeloid leukemia

Simonetta I. Gaumond _, Rama Abdin, Joel Costoya, Andrew V. Schally and Joaquin J. Jimenez

PDF | Full Text | How to cite | Press Release

Oncotarget. 2024; 15:248-254. https://doi.org/10.18632/oncotarget.28579

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Abstract

Simonetta I. Gaumond1, Rama Abdin2, Joel Costoya1, Andrew V. Schally3 and Joaquin J. Jimenez1

1 Dr. Philip Frost Department of Dermatology and Cutaneous Surgery, Miller School of Medicine, University of Miami, Miami, FL 33136, USA

2 Charles E. Schmidt College of Medicine, Florida Atlantic University, Boca Raton, FL 33431, USA

3 Veterans Affairs Medical Center, Miami, FL 33125, USA

Correspondence to:

Simonetta I. Gaumond,

email:

[email protected]

Keywords: leukemia; AML; resistance; growth hormone-releasing hormone; MIA-602

Received: March 06, 2024 Accepted: March 25, 2024 Published: April 08, 2024

Copyright: © 2024 Gaumond et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

ABSTRACT

Acute myeloid leukemia (AML) is characterized by the rapid proliferation of mutagenic hematopoietic progenitors in the bone marrow. Conventional therapies include chemotherapy and bone marrow stem cell transplantation; however, they are often associated with poor prognosis. Notably, growth hormone-releasing hormone (GHRH) receptor antagonist MIA-602 has been shown to impede the growth of various human cancer cell lines, including AML. This investigation examined the impact of MIA-602 as monotherapy and in combination with Doxorubicin on three Doxorubicin-resistant AML cell lines, KG-1A, U-937, and K-562. The in vitro results revealed a significant reduction in cell viability for all treated wild-type cells. Doxorubicin-resistant clones were similarly susceptible to MIA-602 as the wild-type counterpart. Our in vivo experiment of xenografted nude mice with Doxorubicin-resistant K-562 revealed a reduction in tumor volume with MIA-602 treatment compared to control. Our study demonstrates that these three AML cell lines, and their Doxorubicin-resistant clones, are susceptible to GHRH antagonist MIA-602.

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Research Papers:

Exploring the role of GHRH antagonist MIA-602 in overcoming Doxorubicin-resistance in acute myeloid leukemia

Abstract