Bioengineered PLEKHA7 nanodelivery regularly induces behavior alteration and growth retardation of acute myeloid leukemia

• Published in: Biomaterials and biosystems 2022-06, Vol.6, p.100045-100045, Article 100045
• Main Authors: Mohammed, Sameh A., Kimura, Yasuhiro, Toku, Yuhki, Ju, Yang
• Format: Article
• Language: English
• Subjects: Acute myeloid leukemia; Modulator; Nanoparticles; Normal homeostasis; PLEKHA7
• ISSN: 2666-5344; 2666-5344
• DOI: 10.1016/j.bbiosy.2022.100045

•Since the role of PLEKHA7 in acute myeloid leukemia (AML) has not been studied previously, we attempt to demonstrate the correlation between PLEKHA7 expression and the incidence of AML growth.•A bioengineered nanoparticle for PLEKHA7 delivery was developed to regulate the induction of AML behavior alteration and growth retardation induced by efficient PLEKHA7 delivery for recruiting it as a potential target for AML modulation.•This study uncovers that PLEKHA7 is lost or mis-localized for survival and aggressiveness of AML cells. Acute myeloid leukemia (AML) is the most lethal leukemia with an extremely poor prognosis and high relapse rates. In leukemogenesis, adhesion abnormalities can readily guide an imbalance between hematopoietic progenitor cells and bone marrow stromal cells, altering the normal hematopoietic bone marrow microenvironment into leukemic transformation that enhances leukemic proliferation. Here, we have firstly studied the PLEKHA7 expression in leukemic cells to assess their growth capability affected by the restoration of PLEKHA7 in the cells. The efficacy of PLEKHA7-loaded cRGD-mediated PEGylated cationic lipid nanoparticles for efficient PLEKHA7 delivery in leukemic cells as well as the effect of PLEKHA7 on the regulated induction of AML behavior and growth alterations were investigated. PLEKHA7 re-expression diminished colony-forming ability and reinforced the incidence of growth retardation without apoptosis in AML cell lines. PLEKHA7 regulated the restoration of cell surface adhesion and integrity during normal homeostasis. Our findings revealed that PLEKHA7 functions as a behavior and growth modulator in AML. To our knowledge, the role of PLEKHA7 in AML had not been studied previously and our data could be exploited for further mechanistic studies and insights into altering human AML behavior and growth. [Display omitted]