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miRNA-133b targets FGFR1 and presents multiple tumor suppressor activities in osteosarcoma
Gan Gao1, Zhen Tian1, Huan-Ye Zhu1
1Department of Orthopedics, Guizhou Provincial People's Hospital, No. 83, East Zhongshan Road, Guiyang, 550002 Guizhou People's Republic of China.
Background:
Osteosarcoma (OS) is the most common bone malignancy prevalent in children and young adults. MicroRNA-133b (miR-133b), through directly targeting the fibroblast growth factor receptor 1 (FGFR1), is increasingly recognized as a tumor suppressor in different types of cancers. However, little is known on the biological and functional significance of miR-133b/FGFR1 regulation in osteosarcoma.
Methods:
The expressions of miR-133b and FGFR1 were examined by RT-qPCR and compared between 30 paired normal bone tissues and OS tissues, and also between normal osteoblasts and three OS cells lines, MG-63, U2OS, and SAOS-2. Using U2OS and MG-63 as the model system, the functional significance of miR-133b and FGFR1 was assessed on cell viability, proliferation, apoptosis, migration/invasion, and epithelial-mesenchymal transition (EMT) by overexpressing miR-133b and down-regulating FGFR1 expression, respectively. Furthermore, the signaling cascades controlled by miR-133b/FGFR1 were examined.
Results:
miR-133b was significantly down-regulated while FGFR1 robustly up-regulated in OS tissues and OS cell lines, when compared to normal bone tissues and normal osteoblasts, respectively. Low miR-133b expression and high FGFR1 expression were associated with location of the malignant lesion, advanced clinical stage, and distant metastasis. FGFR1 was a direct target of miR-133b. Overexpressing miRNA-133b or knocking down FGFR1 significantly reduced the viability, proliferation, migration/invasion, and EMT, but promoted apoptosis of both MG-63 and U2OS cells. Both the Ras/MAPK and PI3K/Akt intracellular signaling cascades were inhibited in response to overexpressing miRNA-133b or knocking down FGFR1 in OS cells.
Conclusion:
miR-133b, by targeting FGFR1, presents a plethora of tumor suppressor activities in OS cells. Boosting miR-133b expression or reducing FGFR1 expression may benefit OS therapy.
Insights
MicroRNA-133b (miR-133b) acts as a tumor suppressor in osteosarcoma by targeting fibroblast growth factor receptor 1 (FGFR1). Restoring miR-133b or reducing FGFR1 inhibits cancer progression and may offer new therapeutic strategies.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Osteosarcoma (OS) is a primary bone cancer affecting young individuals.
- MicroRNA-133b (miR-133b) is a known tumor suppressor targeting fibroblast growth factor receptor 1 (FGFR1).
- The specific role of miR-133b/FGFR1 in osteosarcoma remains unclear.
Purpose of the Study:
- To investigate the expression and functional significance of miR-133b and FGFR1 in osteosarcoma.
- To elucidate the regulatory relationship between miR-133b and FGFR1 in OS cells.
- To explore the therapeutic potential of targeting the miR-133b/FGFR1 axis in osteosarcoma.
Main Methods:
- Quantitative real-time PCR (RT-qPCR) to assess miR-133b and FGFR1 expression in OS tissues and cell lines.
- Functional assays evaluating cell viability, proliferation, apoptosis, migration, invasion, and epithelial-mesenchymal transition (EMT) upon miR-133b overexpression or FGFR1 knockdown.
- Analysis of intracellular signaling pathways, including Ras/MAPK and PI3K/Akt.
Main Results:
- miR-133b was significantly downregulated, while FGFR1 was upregulated in osteosarcoma tissues and cell lines.
- Low miR-133b and high FGFR1 expression correlated with advanced clinical stage and metastasis.
- Overexpressing miR-133b or downregulating FGFR1 suppressed OS cell viability, proliferation, migration, invasion, and EMT, while promoting apoptosis.
- Both Ras/MAPK and PI3K/Akt signaling pathways were inhibited by miR-133b or FGFR1 modulation.
Conclusions:
- miR-133b exerts tumor suppressor effects in osteosarcoma by targeting FGFR1.
- Modulating the miR-133b/FGFR1 pathway holds promise for osteosarcoma treatment.
- Increasing miR-133b or decreasing FGFR1 expression may represent a viable therapeutic strategy for osteosarcoma.
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