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MicroRNAs, Hypoxia and the Stem-Like State as Contributors to Cancer Aggressiveness
- Source :
- Frontiers in Genetics, Vol 10 (2019), Frontiers in Genetics
- Publication Year :
- 2019
- Publisher :
- Frontiers Media S.A., 2019.
-
Abstract
- MicroRNAs are small non-coding RNA molecules that play key regulatory roles in cancer acting as both oncogenes and tumor suppressors. Due to their potential roles in improving cancer prognostic, predictive, diagnostic and therapeutic approaches, they have become an area of intense research focus in recent years. Several studies have demonstrated an altered expression of several microRNAs under the hypoxic condition and even shown that the hypoxic microenvironment drives the selection of a more aggressive cancer cell population through cellular adaptations referred as the cancer stem-like cell. These minor fractions of cells are characterized by their self-renewal abilities and their ability to maintain the tumor mass, suggesting their crucial roles in cancer development. This review aims to highlight the interconnected role between microRNAs, hypoxia and the stem-like state in contributing to the cancer aggressiveness as opposed to their independent contributions, and it is based in four aggressive tumors, namely glioblastoma, cervical, prostate and breast cancers.
- Subjects :
- 0301 basic medicine
lcsh:QH426-470
Population
Cell
Review
Biology
stem-like state
law.invention
03 medical and health sciences
0302 clinical medicine
Prostate
law
microRNA
medicine
Genetics
cancer
education
Genetics (clinical)
education.field_of_study
hypoxia
RNA
Hypoxia (medical)
microenvironment
microRNAs
cancer aggressiveness
lcsh:Genetics
030104 developmental biology
medicine.anatomical_structure
030220 oncology & carcinogenesis
Cancer research
Molecular Medicine
Suppressor
Cancer development
medicine.symptom
Subjects
Details
- Language :
- English
- ISSN :
- 16648021
- Volume :
- 10
- Database :
- OpenAIRE
- Journal :
- Frontiers in Genetics
- Accession number :
- edsair.doi.dedup.....8c02b691fcd1cadf3d43a3fc9a6de735
- Full Text :
- https://doi.org/10.3389/fgene.2019.00125/full