Expression analysis and function of mitochondrial genome-encoded microRNAs

Author:

Kuthethur Raviprasad1ORCID,Shukla Vaibhav1,Mallya Sandeep2,Adiga Divya1,Kabekkodu Shama Prasada1,Ramachandra Lingadakai3,Saxena P. U. Prakash4,Satyamoorthy Kapaettu1,Chakrabarty Sanjiban1ORCID

Affiliation:

1. Department of Cell and Molecular Biology, Manipal School of Life Sciences, Manipal Academy of Higher Education, Manipal, Karnataka, 576104, India

2. Department of Bioinformatics, Manipal School of Life Sciences, Manipal Academy of Higher Education, Manipal, Karnataka, 576104, India

3. Department of Surgery, Kasturba Medical College, Manipal Academy of Higher Education, Manipal, Karnataka, 576104, India

4. Department of Radiation Oncology, Kasturba Medical College, Manipal Academy of Higher Education, Mangalore, Karnataka, 575001, India

Abstract

ABSTRACT MicroRNAs (miRNAs) play a significant role in nuclear and mitochondrial anterograde and retrograde signaling. Most of the miRNAs found inside mitochondria are encoded in the nuclear genome, with a few mitochondrial genome-encoded non-coding RNAs having been reported. In this study, we have identified 13 mitochondrial genome-encoded microRNAs (mitomiRs), which were differentially expressed in breast cancer cell lines (MCF-7, MDA-MB-468 and MDA-MB-231), non-malignant breast epithelial cell line (MCF-10A), and normal and breast cancer tissue specimens. We found that mitochondrial DNA (mtDNA) depletion and inhibition of mitochondrial transcription led to reduced expression of mitomiRs in breast cancer cells. MitomiRs physically interacted with Ago2, an RNA-induced silencing complex (RISC) protein, in the cytoplasm and inside mitochondria. MitomiRs regulate the expression of both nuclear and mitochondrial transcripts in breast cancer cells. We showed that mitomiR-5 targets the PPARGC1A gene and regulates mtDNA copy number in breast cancer cells. MitomiRs identified in the present study may be a promising tool for expression and functional analysis in patients with a defective mitochondrial phenotype, including cancer and metabolic syndromes. This article has an associated First Person interview with the first author of the paper.

Funder

Science and Engineering Research Board

Indian Council of Medical Research

Department of Science and Technology, Ministry of Science and Technology, India

Technology Information, Forecasting and Assessment Council

Vision Group on Science and Technology

Karnataka Fund for Infrastructure Strengthening in Science and Technology

Manipal Academy of Higher Education

Publisher

The Company of Biologists

Subject

Cell Biology

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