MicroRNA-122 mimic/microRNA-221 inhibitor combination as a novel therapeutic tool against hepatocellular carcinoma

Theodor Bilharz Research Institute

Bibliographic Information

Authors: Hassan M.; Elzallat M.; Aboushousha T.; Elhusseny Y.; El-Ahwany E.

Journal: Non-coding RNA Research

Publisher: KeAi Communications Co.

Publication Date: March 2023

Volume / Issue: Volume 8 / Issue 1

Pages: 126–134

ISSN: 24680540

DOI: 10.1016/j.ncrna.2022.11.005

Scopus: View on Scopus

Document Type: Article

Access: All Open Access; Gold Open Access; Green Open Access

Authors and Affiliations

Hassan M., Immunology Department, Theodor Bilharz Research Institute, Giza, Egypt; Elzallat M., Immunology Department, Theodor Bilharz Research Institute, Giza, Egypt; Aboushousha T., Pathology Department, Theodor Bilharz Research Institute, Giza, Egypt; Elhusseny Y., School of Medicine, NewGiza University, Giza, Egypt; El-Ahwany E., Immunology Department, Theodor Bilharz Research Institute, Giza, Egypt

Abstract

Background: Therapeutic microRNAs (miRNAs) delivery holds a lot of promise for treating human malignancies. So, this study was carried out to examine the potential of miR-122 mimic and/or miR-221 inhibitor as an innovative therapeutic strategy for HCC in an animal model. Methodology: Mice were categorized into five groups comprising: (1) a normal control group, (2) an HCC group subjected to diethylnitrosamine (DEN) injection for 12 weeks, (3) a miR-122 mimic-treated HCC group, (4) a miR-221 inhibitor-treated HCC group, and (5) a miR-122 mimic/miR-221 inhibitor-treated HCC group. After 16 weeks, all animals were sacrificed and underwent biochemical, miRNAs and genes expression, histopathological, and immunohistochemical examinations. Results: The miR-122 mimic/miR-221 inhibitor combination dramatically reduced the levels of pro-inflammatory, liver cancer, angiogenesis, and cell proliferation markers when compared to either treatment alone. It also down-regulated the expression of cyclin D1, TGF-β, and β-catenin genes, which are involved in promoting cell cycle progression and cancer cell proliferation. Furthermore, it caused the resolution of nearly all the histological malignant features as well as the reduction of malignant cellular markers, including α-smooth muscle actin, arginase-1, and tropomyosin-1. Conclusions: The co-treatment with miR-122 mimic and miR-221 inhibitor amplifies the benefits of either treatment on HCC through targeting the SENP1 and ARF4 genes, respectively. This combination can inhibit cancer cell proliferation and angiogenesis while inducing tumor apoptosis and necrosis. This study demonstrates the therapeutic potential of reversing a dysregulated miRNAs expression pattern in HCC. As a result, future research should concentrate on turning miRNA understanding into therapeutic applications. © 2022 The Authors

Keywords

ARF4; Diethylnitrosamine; Hepatocellular carcinoma; miRNA; SENP1; adenosine diphosphate ribosylation factor 4; alpha fetoprotein; alpha smooth muscle actin; alpha tropomyosin; arginase 1; beta catenin; cyclin D1; microRNA; microRNA 122; microRNA 221; platelet derived growth factor; sodium chloride; transforming growth factor beta; tumor necrosis factor; vasculotropin; angiogenesis; animal experiment; animal model; animal tissue; apoptosis; Article; bone marrow mesenchymal stem cell; cell cycle progression; cell proliferation; cell viability; controlled study; cytotoxicity; epithelial mesenchymal transition; gene expression; immunohistochemistry; liver cancer; liver cell carcinoma; male; mouse; necrosis; nonhuman

Citation Information

Scopus Citations: 33

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