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SNHG16 promotes osteosarcoma progression and enhances cisplatin resistance by sponging miR-16 to upregulate ATG4B
Yu Liu1, Sanjun Gu1, Haifeng Li1
1Department of Orthopaedics, The Ninth People's Hospital of Wuxi City, Wuxi, Jiangsu, PR China.
Background:
Human osteosarcoma is the most common primary cancer of the bone. Multiple mechanisms underlying cell growth, apoptosis, bone development, and drug resistance are important in the development of osteosarcoma therapy, which remains to be fully studied.
Methods:
We collected thirty-paired tumor tissues and the adjacent normal ones from osteosarcoma patients. Two osteosarcoma cell lines (SAOS2, U2OS) were used for in vitro experiments. RT-qPCR and Western blot were used for gene expression detection. We applied starBase to predict the potential binding sites. Then, the luciferase reporter assay was used to confirm the potential direct interaction. Besides, we applied CCK-8, EdU assay, and flow cytometric assays to detect cell growth and apoptosis rate. We used wound healing and transwell assays to determine cell migration and invasion abilities. Additionally, we constructed a cisplatin-resistant osteosarcoma cell line to study the potential impact of the regulatory axis on drug resistance.
Results:
Small nucleolar RNA host gene 16 (SNHG16) and autophagy-related 4B (ATG4B) were significantly upregulated in osteosarcoma tissues than the normal ones, and the higher expression level of SNHG16 predicted a poor prognosis in osteosarcoma patients. By contrast, the expression level of miR-16 was markedly lower in tumor tissues and was negatively correlated with SNHG16 (p < 0.001). SNHG16 was shown to promote cell growth, migration, and invasion, while miR-16 reversed this impact. Meanwhile, overexpression of ATG4B significantly promoted the development of osteosarcoma cells attenuated by SNHG16 knockdown or miR-16 mimics. Specifically, overexpression of ATG4B promoted cisplatin-induced autophagy and inhibited cell apoptosis rate, which enhanced the cisplatin resistance in osteosarcoma cell lines.
Conclusions:
Overall, our findings showed the importance of the regulatory axis of SNHG16/miR-16/ATG4B underlying osteosarcoma progression and chemoresistance to cisplatin. This research would benefit the therapy development in the treatment of osteosarcoma.
Insights
This study reveals the SNHG16/miR-16/ATG4B axis promotes osteosarcoma progression and cisplatin resistance. Targeting this pathway may improve osteosarcoma therapy and overcome drug resistance.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Human osteosarcoma is a common bone cancer with complex underlying mechanisms.
- Understanding cell growth, apoptosis, bone development, and drug resistance is crucial for effective osteosarcoma therapy.
Purpose of the Study:
- To investigate the regulatory role of the SNHG16/miR-16/ATG4B axis in osteosarcoma progression.
- To explore the impact of this axis on chemoresistance to cisplatin.
Main Methods:
- Gene expression analysis (RT-qPCR, Western blot) in osteosarcoma tissues and cell lines.
- In vitro assays including cell proliferation, migration, invasion, and apoptosis.
- Luciferase reporter assay to confirm direct interactions.
- Construction of a cisplatin-resistant cell line to assess drug resistance mechanisms.
Main Results:
- SNHG16 and ATG4B were upregulated, while miR-16 was downregulated in osteosarcoma.
- SNHG16 promoted cell growth, migration, and invasion; miR-16 reversed these effects.
- ATG4B overexpression enhanced cisplatin resistance by promoting autophagy and inhibiting apoptosis.
Conclusions:
- The SNHG16/miR-16/ATG4B regulatory axis is critical for osteosarcoma progression and cisplatin resistance.
- This axis represents a potential therapeutic target for improving osteosarcoma treatment outcomes.
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