Epigallocatechin-3-gallate Enhances the Efficacy of MicroRNA-34a Mimic and MicroRNA-93 Inhibitor Co-transfection in Prostate Cancer Cell Line.


Journal

Iranian journal of allergy, asthma, and immunology
ISSN: 1735-5249
Titre abrégé: Iran J Allergy Asthma Immunol
Pays: Iran
ID NLM: 101146178

Informations de publication

Date de publication:
19 Dec 2020
Historique:
received: 22 06 2020
accepted: 03 08 2020
entrez: 19 1 2021
pubmed: 20 1 2021
medline: 1 10 2021
Statut: epublish

Résumé

The potential role of microRNAs (miRNA or MIR) as therapeutic molecules has moved them from basic research to the field of cancer therapy. High expression of miR-93 and low expression of miR-34a have previously been indicated in prostate cancer (PC), which is the second leading cause of cancer-related death in men. Androgen receptor (AR) and prostate-specific antigen (PSA) play key roles in the initiation and progression of this cancer. Therefore, this study aimed to investigate the effects of the transfection and co-transfection of miR-34a mimic and miR-93 inhibitor with or without epigallocatechin-3-gallate (EGCG) on prostate cancer cell line and also to evaluate their effects on the expression of AR, PSA. Human lymph node carcinoma of the prostate (LNCaP) cells were treated with miR-34a mimic or/and miR-93 inhibitor with or without EGCG. Gene or protein expressions were assessed by real-time PCR or western blotting of lysates. The transfection with miR-34a mimics significantly reduced the mRNA expression of AR (p=0.0016), and PSA (p=0.038) compared to the control. Also, the miR-93 inhibitor led to a decrease in the mRNA expression of AR (p=0.0057) and PSA (p>0.05) compared to the control group. Furthermore, the co-transfection, along with EGCG, caused more decrease in both the AR (p<0.001) and the PSA (p=0.003) expression compared with the co-transfection without EGCG. Our study indicates that the reduced expression of AR and PSA in PC cells followed by treatment with miR-34a mimic and miR-93 inhibitor and their combination with EGCG as a natural substance may be a promising therapeutic way for controlling the growth of these malignant cells.

Identifiants

pubmed: 33463130
doi: 10.18502/ijaai.v19i6.4930
doi:

Substances chimiques

MIRN34 microRNA, human 0
MIRN93 microRNA, human 0
MicroRNAs 0
Receptors, Androgen 0
Catechin 8R1V1STN48
epigallocatechin gallate BQM438CTEL
Prostate-Specific Antigen EC 3.4.21.77

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

612-623

Auteurs

Hossein Mokhtari (H)

Department of Clinical Biochemistry, Faculty of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. mokhtarimsh@yahoo.com.

Bahram Yaghmaei (B)

Department of Clinical Biochemistry, Faculty of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. yaghmaeib@sbmu.ac.ir.

Majid Sirati-Sabet (M)

Department of Clinical Biochemistry, Faculty of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. sirati@sbmu.ac.ir.

Narjes Jafari (N)

Department of Immunology, Faculty of Medicine, Immunogenetics Research Center, Mazandaran University of Medical Sciences, Sari, Iran. sn.jafari@gmail.com.

Alireza Mardomi (A)

Department of Immunology, Faculty of Medicine, Immunogenetics Research Center, Mazandaran University of Medical Sciences, Sari, Iran. abedianks@alumnus.tums.ac.ir.

Saeid Abediankenari (S)

Department of Immunology, Faculty of Medicine, Immunogenetics Research Center, Mazandaran University of Medical Sciences, Sari, Iran. abedianks@alumnus.tums.ac.ir.

Abdolkarim Mahrooz (A)

Molecular and Cell Biology Research Center, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran. amahrooz@mazums.ac.ir.

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Classifications MeSH