Related Experiment Video
Updated: Oct 22, 2025
Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
MicroRNAs as Potential Predictors of Response to CDK4/6 Inhibitor Treatment
Angeliki Andrikopoulou1, Almog Shalit2, Eleni Zografos1
1Department of Clinical Therapeutics, Alexandra Hospital, Medical School, 11528 Athens, Greece.
Abstract:
Cyclin-dependent kinase 4/6 (CDK4/6) inhibitors have emerged as novel treatment options in the management of advanced or metastatic breast cancer. MicroRNAs are endogenous non-coding 19-22-nucleotide-long RNAs that regulate gene expression in development and tumorigenesis. Herein, we systematically review all microRNAs associated with response to CDK4/6 inhibitors in solid tumors and hematological malignancies. Eligible articles were identified by a search of the MEDLINE and ClinicalTrials.gov databases for the period up to1 January 2021; the algorithm consisted of a predefined combination of the words "microRNAs", "cancer" and "CDK 4/6 inhibitors". Overall, 15 studies were retrieved. Six microRNAs (miR-126, miR-326, miR3613-3p, miR-29b-3p, miR-497 and miR-17-92) were associated with sensitivity to CDK4/6 inhibitors. Conversely, six microRNAs (miR-193b, miR-432-5p, miR-200a, miR-223, Let-7a and miR-21) conferred resistance to treatment with CDK4/6 inhibitors. An additional number of microRNAs (miR-124a, miR9, miR200b and miR-106b) were shown to mediate cellular response to CDK4/6 inhibitors without affecting sensitivity to treatment. Collectively, our review provides evidence that microRNAs could serve as predictive biomarkers for treatment with CDK4/6 inhibitors. Moreover, microRNA-targeted therapy could potentially maximize sensitivity to CDK4/6 inhibition.
Insights
MicroRNAs can predict response to cyclin-dependent kinase 4/6 (CDK4/6) inhibitors in cancer. Certain microRNAs indicate sensitivity, while others confer resistance, suggesting potential for microRNA-targeted therapies.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Cyclin-dependent kinase 4/6 (CDK4/6) inhibitors are emerging treatments for advanced or metastatic breast cancer.
- MicroRNAs (miRNAs) are small non-coding RNAs regulating gene expression in biological processes, including cancer development.
- Understanding miRNA roles in CDK4/6 inhibitor response is crucial for optimizing cancer therapy.
Purpose of the Study:
- To systematically review microRNAs associated with response to CDK4/6 inhibitors in solid tumors and hematological malignancies.
- To identify specific miRNAs that predict sensitivity or resistance to CDK4/6 inhibitor therapy.
- To explore the potential of miRNAs as predictive biomarkers and therapeutic targets in CDK4/6 inhibitor treatment.
Main Methods:
- A systematic literature search was conducted on MEDLINE and ClinicalTrials.gov databases up to January 1, 2021.
- The search algorithm combined keywords: "microRNAs", "cancer", and "CDK 4/6 inhibitors".
- Fifteen eligible studies were retrieved and analyzed for miRNA associations with CDK4/6 inhibitor response.
Main Results:
- Six miRNAs (miR-126, miR-326, miR3613-3p, miR-29b-3p, miR-497, miR-17-92) were linked to sensitivity to CDK4/6 inhibitors.
- Six miRNAs (miR-193b, miR-432-5p, miR-200a, miR-223, Let-7a, miR-21) were associated with resistance to CDK4/6 inhibitors.
- Additional miRNAs (miR-124a, miR9, miR200b, miR-106b) mediated cellular response without affecting treatment sensitivity.
Conclusions:
- MicroRNAs show promise as predictive biomarkers for CDK4/6 inhibitor treatment efficacy.
- Targeting specific microRNAs could potentially enhance patient sensitivity to CDK4/6 inhibition.
- Further research into miRNA-mediated mechanisms may lead to improved cancer treatment strategies.
Related Concept Videos
02:34Inhibition of Cdk Activity
02:15M-Cdk Drives Transition Into Mitosis
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
03:03mTOR Signaling and Cancer Progression
The mTOR pathway or the...