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Intratibial Osteosarcoma Cell Injection to Generate Orthotopic Osteosarcoma and Lung Metastasis Mouse Models
Published on: October 28, 2021
miR-342-5p inhibits osteosarcoma cell growth, migration, invasion, and sensitivity to Doxorubicin through targeting
Qing Liu1, Zhenting Wang1, Xiaohua Zhou2
1Department of Spine Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Abstract:
Osteosarcoma (OS) accounts for 9 percent of cancer-related deaths in young people. The PI3K/Akt signaling, a well-known carcinogenic signaling pathway in human cancer, cooperates with other signaling pathways such as Wnt signaling to promote cancer progression. Wnt7b, as a transforming member of the Wnt family, could activate mTORC1 through PI3K-AKT signaling and is upregulated in OS. In the present study, we found that miR-342-5p inhibits Wnt7b expression via direct binding to Wnt7b 3'-UTR. miR-342-5p overexpression remarkably suppressed the viability and invasion while enhanced the apoptosis of OS cells; meanwhile, Wnt7b, β-catenin, c-myc, and cyclin D1 proteins were reduced while E-cadherin protein showed to be increased. Consistent with its expression pattern, Wnt7b exerted oncogenic effects on OS cells. Wnt7b could significantly attenuate the impacts of miR-342-5p. In conclusion, we demonstrated a miR-342-5p/Wnt7b axis that regulates the capacity of OS cells to proliferate and to invade through Wnt/β-catenin signaling. The miR-342-5p/Wnt7b axis might be novel targets for OS targeted therapy, which needs further in vivo and clinical investigations.
Insights
MicroRNA-342-5p inhibits osteosarcoma progression by targeting Wnt7b. This miR-342-5p/Wnt7b axis regulates cell proliferation and invasion, offering potential therapeutic targets for osteosarcoma.
Area of Science:
- Oncology
- Molecular Biology
- Gene Regulation
Background:
- Osteosarcoma (OS) is a significant cause of cancer-related mortality in young individuals.
- The PI3K/Akt and Wnt signaling pathways are implicated in cancer progression, with Wnt7b being upregulated in OS.
- Wnt7b activates mTORC1 via PI3K-AKT signaling, contributing to tumor development.
Purpose of the Study:
- To investigate the role of miR-342-5p in osteosarcoma.
- To elucidate the regulatory relationship between miR-342-5p and Wnt7b in OS cells.
- To explore the potential of the miR-342-5p/Wnt7b axis as a therapeutic target for OS.
Main Methods:
- In vitro studies involving miR-342-5p overexpression in OS cells.
- Analysis of Wnt7b expression and its interaction with miR-342-5p.
- Assessment of cell viability, invasion, apoptosis, and protein levels (Wnt7b, β-catenin, c-myc, cyclin D1, E-cadherin).
Main Results:
- miR-342-5p directly inhibits Wnt7b expression by binding to its 3'-UTR.
- Overexpression of miR-342-5p suppressed OS cell viability and invasion while enhancing apoptosis.
- miR-342-5p overexpression led to decreased Wnt7b, β-catenin, c-myc, and cyclin D1, and increased E-cadherin.
- Wnt7b counteracted the effects of miR-342-5p, exhibiting oncogenic properties.
Conclusions:
- A novel miR-342-5p/Wnt7b regulatory axis was identified in osteosarcoma.
- This axis controls OS cell proliferation and invasion through the Wnt/β-catenin signaling pathway.
- The miR-342-5p/Wnt7b axis represents a potential novel target for osteosarcoma-specific therapies, warranting further investigation.
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