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Detection of Mitochondria Membrane Potential to Study CLIC4 Knockdown-induced HN4 Cell Apoptosis In Vitro
Published on: July 17, 2018
MicroRNA: a connecting road between apoptosis and cholesterol metabolism
Yogita K Adlakha1, Neeru Saini2
1Cellular and Molecular Neuroscience, National Brain Research Centre, Manesar, 122051, India. yogita@nbrc.ac.in.
Abstract:
Resistance to apoptosis leads to tumorigenesis and failure of anti-cancer therapy. Recent studies also highlight abrogated lipid/cholesterol metabolism as one of the root causes of cancer that can lead to metastatic transformations. Cancer cells are dependent on tremendous supply of cellular cholesterol for the formation of new membranes and continuation of cell signaling. Cholesterol homeostasis network tightly regulates this metabolic need of cancer cells on cholesterol and other lipids. Genetic landscape is also shared between apoptosis and cholesterol metabolism. MicroRNAs (miRNAs) are the new fine tuners of signaling pathways and cellular processes and are known for their ability to post-transcriptionally repress gene expression in a targeted manner. This review summarizes the current knowledge about the cross talk between apoptosis and cholesterol metabolism via miRNAs. In addition, we also emphasize herein recent therapeutic modulations of specific miRNAs and their promising potential for the treatment of deadly diseases including cancer and cholesterol related pathologies. Understanding of the impact of miRNA-based regulation of apoptosis and metabolic processes is still at its dawn and needs further research for the development of future miRNA-based therapies. As both these physiological processes affect cellular homeostasis, we believe that this comprehensive summary of miRNAs modulating both apoptosis and cholesterol metabolism will open uncharted territory for scientific exploration and will provide the foundation for discovering novel drug targets for cancer and metabolic diseases.
Insights
MicroRNAs (miRNAs) regulate both apoptosis and cholesterol metabolism, crucial processes in cancer development. Understanding this crosstalk offers new therapeutic targets for cancer and metabolic diseases.
Area of Science:
- Molecular Biology
- Cell Biology
- Biochemistry
Background:
- Resistance to apoptosis and altered lipid/cholesterol metabolism are hallmarks of cancer, contributing to tumorigenesis and therapeutic failure.
- Cancer cells exhibit high dependence on cholesterol for membrane biogenesis and signaling, necessitating tight regulation by the cholesterol homeostasis network.
- Shared genetic landscapes exist between apoptosis regulation and cholesterol metabolism pathways.
Purpose of the Study:
- To review the intricate crosstalk between apoptosis and cholesterol metabolism mediated by microRNAs (miRNAs).
- To highlight recent therapeutic strategies involving miRNA modulation for cancer and cholesterol-related pathologies.
- To underscore the nascent stage of understanding miRNA-based regulation in these processes and its therapeutic potential.
Main Methods:
- Literature review focusing on studies investigating the interplay between miRNAs, apoptosis, and cholesterol metabolism.
- Analysis of genetic and regulatory mechanisms connecting these pathways.
- Synthesis of current knowledge on miRNA-based therapeutic interventions.
Main Results:
- MicroRNAs (miRNAs) act as key post-transcriptional regulators influencing both apoptosis and cholesterol homeostasis.
- Specific miRNAs have been identified that modulate the expression of genes involved in both cellular death and lipid metabolism.
- Dysregulation of these miRNAs is implicated in the progression of cancer and metabolic disorders.
Conclusions:
- The interplay between apoptosis and cholesterol metabolism, orchestrated by miRNAs, is a critical determinant of cellular homeostasis.
- Targeting specific miRNAs presents a promising avenue for developing novel therapies against cancer and metabolic diseases.
- Further research into miRNA-mediated regulation is essential for advancing future therapeutic strategies.
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