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Updated: Jan 24, 2026
Three-Dimensional Bone Extracellular Matrix Model for Osteosarcoma
Published on: April 12, 2019
LncRNA SNHG7 participates in osteosarcoma progression by down-regulating p53 via binding to DNMT1
1Department of Sport Medicine, Yantaishan Hospital, Yantai, China. L577iyu@163.com.
Objective:
This study aims to explore the role of lncRNA SNHG7 in the development of osteosarcoma, and its underlying mechanism.
Patients And Methods:
The quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed to detect SNHG7 expression in tumor tissues and paracancerous tissues harvested from osteosarcoma patients. Meanwhile, the relationship between SNHG7 expression and tumorigenesis was analyzed. The effects of SNHG7 and p53 on cell proliferation, cell cycle and apoptosis were detected by plate cloning and flow cytometry, respectively. The binding relationship between SNHG7 and DNMT1, as well as the regulatory mechanism of DNMT1 on p53, were detected by RIP and ChIP. Western blot was conducted to detect the expression of p53 after the knockdown of SNHG7 in osteosarcoma cells. Rescue experiments were finally conducted to verify whether SNHG7 exerted its biological function by targeting p53.
Results:
QRT-PCR results demonstrated that the expression of SNHG7 in osteosarcoma tissues was remarkably higher than that in paracancerous tissues. Moreover, SNHG7 expression in osteosarcoma with stage III and IV was higher than those in stage I and II. The inhibition of SNHG7 in osteosarcoma cells U2OS and HOS promoted cell proliferation, arrested cell cycle in the G0/G1 phase and induced apoptosis. RIP and ChIP experiments illustrated that SNHG7 inhibited the expression of p53 by binding to DNMT1. The overexpression of p53 in U2OS cells partially reversed the promoted cell proliferation and apoptosis caused by SNHG7.
Conclusions:
Highly expressed SNHG7 can promote the proliferation and inhibit apoptosis of osteosarcoma cells by regulating p53 expression by binding to DNMT1.
Insights
Long non-coding RNA SNHG7 promotes osteosarcoma progression by inhibiting p53. This study reveals SNHG7 as a potential therapeutic target for osteosarcoma, impacting cell proliferation and apoptosis.
Area of Science:
- Oncology
- Molecular Biology
- Epigenetics
Background:
- Osteosarcoma is a primary bone malignancy with complex molecular underpinnings.
- Long non-coding RNAs (lncRNAs) are increasingly recognized for their roles in cancer development.
- The specific function of lncRNA SNHG7 in osteosarcoma remains to be fully elucidated.
Purpose of the Study:
- To investigate the role of lncRNA SNHG7 in osteosarcoma pathogenesis.
- To elucidate the molecular mechanism by which SNHG7 influences osteosarcoma progression.
- To explore SNHG7 as a potential therapeutic target.
Main Methods:
- Quantitative Real-Time Polymerase Chain Reaction (qRT-PCR) to assess SNHG7 expression levels.
- Cell proliferation, cell cycle, and apoptosis assays (plate cloning, flow cytometry).
- RNA immunoprecipitation (RIP), Chromatin immunoprecipitation (ChIP), and Western blot to determine molecular interactions and regulatory pathways.
Main Results:
- SNHG7 expression is significantly upregulated in osteosarcoma tissues, correlating with advanced tumor stage.
- Inhibition of SNHG7 suppresses cell proliferation, induces apoptosis, and arrests the cell cycle.
- SNHG7 binds to DNMT1, inhibiting p53 expression and promoting osteosarcoma cell growth.
Conclusions:
- High SNHG7 expression drives osteosarcoma proliferation and inhibits apoptosis by downregulating p53 via DNMT1.
- SNHG7 represents a potential diagnostic marker and therapeutic target for osteosarcoma.
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