Emerging role of m6A modification in ovarian cancer: progression, drug resistance, and therapeutic prospects
These videos have been matched automatically. Contact us if they are not relevant.
These videos have been matched automatically. Contact us if they are not relevant.
View abstract on PubMed
Summary
This summary is machine-generated.N6-methyladenosine (m6A) RNA modifications are crucial in ovarian cancer (OC) development and drug resistance. Targeting these epitranscriptomic changes offers new therapeutic strategies for this challenging malignancy.
Area Of Science
- Oncology
- Molecular Biology
- Epigenetics
Background
- Ovarian cancer (OC) is a leading cause of cancer mortality in women, with poor prognosis due to treatment limitations like chemotherapy resistance and tumor relapse.
- Current OC treatments are often broadly cytotoxic, necessitating a move towards targeted therapies based on unique molecular characteristics.
Purpose Of The Study
- To review the role of N6-methyladenosine (m6A) modifications in coding and non-coding RNAs in ovarian cancer.
- To highlight m6A modifications as potential prognostic markers and therapeutic targets in OC.
Main Methods
- Literature review focusing on epitranscriptomic regulation, specifically m6A modifications in OC.
- Analysis of the impact of m6A on OC development, migration, invasion, and drug resistance.
Main Results
- m6A modifications are frequently disrupted in OC, impacting various cellular processes.
- m6A regulators (writers, erasers, readers) play critical roles in OC progression and response to therapy.
Conclusions
- m6A modifications are pivotal in OC pathogenesis and represent promising prognostic biomarkers.
- Targeting RNA-modified regulators offers a novel therapeutic avenue for overcoming OC treatment challenges.
These videos have been matched automatically. Contact us if they are not relevant.
These videos have been matched automatically. Contact us if they are not relevant.
Related Concept Videos
Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
MicroRNA (miRNA) are short, regulatory RNA transcribed from introns (non-coding regions of a gene) or intergenic regions (stretches of DNA present between genes). Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself, forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA...