ArticleAnti-cancer agents in medicinal chemistry2014
MiR-138 and MiR-135 directly target focal adhesion kinase, inhibit cell invasion, and increase sensitivity to chemotherapy in cancer cells.
Article in Anti-cancer agents in medicinal chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 56 citations in OpenAlex.
- MicroRNA-138 regulates hypoxia-induced endothelial cell dysfunction by targeting S100A1.PloS one · 2013Trial
- MicroRNA-138 regulation promotes the efficacy of oncolytic herpes virus G47Δ for malignant brain tumor therapy.Molecular therapy. Oncology · 2026Article
- The Role of miR-138 in Cardiovascular Diseases.BioMed research international · 2025Review
- MicroRNA-138: an emerging regulator of skeletal development, homeostasis, and disease.American journal of physiology. Cell physiology · 2023Review
- Expression of pY397-FAK and Its miR Regulators Drive Dedifferentiation in the Thyroid Neoplasia Spectrum.Cells · 2023Article
- A review on the importance of miRNA-135 in human diseases.Frontiers in genetics · 2022Review
- MicroRNA-138 Abates Fibroblast Motility With Effect on Invasion of Adjacent Cancer Cells.Frontiers in oncology · 2022Article
- Article
- 5-Fluorouracil: A Narrative Review on the Role of Regulatory Mechanisms in Driving Resistance to This Chemotherapeutic Agent.Frontiers in oncology · 2021Review
- miR-135a Reduces Osteosarcoma Pulmonary Metastasis by Targeting Both BMI1 and KLF4.Frontiers in oncology · 2021Article
- MiRNAs as Anti-Angiogenic Adjuvant Therapy in Cancer: Synopsis and Potential.Frontiers in oncology · 2021Review
- Review
- Correlation between miR-138-5p expression and efficacy of platinum-based chemotherapy in advanced gastric cancer patients.Translational cancer research · 2020Article
- CircNOL10 Acts as a Sponge of miR-135a/b-5p in Suppressing Colorectal Cancer Progression via Regulating KLF9.OncoTargets and therapy · 2020Article
- MiR-138 Suppresses the PDK1 Expression to Decrease the Oxaliplatin Resistance of Colorectal Cancer.OncoTargets and therapy · 2020Article
- Expression of miR-23a and miR-135 and tumor markers in gastric cancer patients and the significance in diagnosis.Oncology letters · 2019Article
- Sulforaphane Induces miR135b-5p and Its Target Gene, RASAL2, thereby Inhibiting the Progression of Pancreatic Cancer.Molecular therapy oncolytics · 2019Article
- miR-21 facilitates the diagnostic value of miR-138 for papillary thyroid cancer in formalin-fixed paraffin-embedded tissues.Translational cancer research · 2019Article
- Article
- Pivotal role of microRNA-138 in human cancers.American journal of cancer research · 2019Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Focal Adhesion Kinase is a 125 kDa non-receptor kinase and overexpressed in many types of tumors. Recently, short noncoding RNAs, called microRNAs have been discovered as regulators of gene expression mainly through binding to the untranslated region (UTR) of mRNA. In this report we show that MiR-138 and MiR-135 down-regulated FAK expression in cancer cells. MiR-138 and MiR-135 inhibited FAK protein expression in different cancer cell lines. The computer analysis of 3'FAK-untranslated region (FAKUTR) identified one conserved MiR-138 binding site (CACCAGCA) at positions 3514-3521 and one conserved MiR-135 (AAGCCAU) binding site at positions 4278-4284 in the FAK-UTR. By a dual-luciferase assay we demonstrate that MiR-138 and MiR-135 directly bound the FAK untranslated region using FAK-UTR-Target (FAK-UTR) luciferase plasmid and inhibited its luciferase activity. The sitedirected mutagenesis of the MiR-138 and MiR-135 binding sites in the FAK-UTR abrogated MiR-138 and MiR-135-directed inhibition of FAK-UTR. Real-time PCR demonstrated that cells transfected with MiR-138 and MiR-135 expressed decreased FAK mRNA levels. Moreover, stable expression of MiR-138 and MiR-135 in 293 and HeLa cells decreased cell invasion and increased sensitivity to 5- fluorouracil (5-FU), FAK inhibitor, Y15, and doxorubicin. In addition, MiR-138 significantly decreased 293 xenograft tumor growth in vivo. This is the first report on regulation of FAK expression by MiR-135 and MiR138 that affected invasion, drug sensitivity, and tumor growth in cancer cells, which is important to the development of FAK-targeted therapeutics and understanding their novel regulations and functions.
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