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Updated: Feb 19, 2026
Author Spotlight: RNA FISH for Locating lncRNA-SNHG6 in Osteosarcoma Cells
Published on: June 16, 2023
Long non-coding RNA SNHG1 regulates NOB1 expression by sponging miR-326 and promotes tumorigenesis in osteosarcoma
Jiandong Wang1, Lei Cao1, Jianhong Wu1
1Department of Trauma and Orthopedics, Trauma Emergency Center, Shanghai General Hospital, Shanghai Jiao Tong University, Shanghai 200080, P.R. China.
Abstract:
The long non-coding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) has been demonstrated to participate in the deterioration of many types of cancer. However, the underlying mechanisms of SNHG1-mediating functions in osteosarcoma (OS) have yet to be elucidated. In the present study, our results showed that SNHG1 was upregulated in OS tissues and cell lines, and high SNHG1 expression predicts poor overall survival of OS patients. Knockdown of SNHG1 inhibited cell growth and metastasis of OS in vitro and in vivo. Furthermore, our data demonstrated that there was reciprocal repression between SNHG1 and miR-326 which act as a tumor suppressor in OS cells, and exhibiting a strong negative relationship between SNHG1 and miR-326 expression in OS tissues. Additionally, we identified that SNHG1 increased human nin one binding protein (NOB1), an oncogene, through sponging miR-326 as competing endogenous RNA (ceRNA), finally prompting cell growth, migration and invasion in OS. Collectively, these findings not only uncovered that the SNHG1/miR-326/NOB1 signaling axis has a key role in OS progression but also suggested the potential application of SNHG1 and miR-326 as biomarkers in the OS diagnosis and treatment.
Insights
The long non-coding RNA SNHG1 promotes osteosarcoma (OS) growth and metastasis by interacting with miR-326 and NOB1. Targeting SNHG1 may offer new therapeutic strategies for OS patients.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Osteosarcoma (OS) is a primary bone malignancy with poor prognosis.
- Long non-coding RNAs (lncRNAs) are increasingly recognized for their roles in cancer progression.
- The specific functions of SNHG1 in OS remain largely unknown.
Purpose of the Study:
- To investigate the role and mechanism of SNHG1 in osteosarcoma.
- To explore the relationship between SNHG1, miR-326, and NOB1 in OS.
- To evaluate SNHG1 and miR-326 as potential diagnostic and therapeutic targets for OS.
Main Methods:
- Quantitative real-time PCR (qRT-PCR) to measure gene expression.
- In vitro and in vivo experiments to assess cell growth, migration, and invasion.
- Bioinformatic analysis and luciferase reporter assays to confirm molecular interactions.
Main Results:
- SNHG1 was significantly upregulated in OS tissues and cell lines, correlating with poor patient survival.
- SNHG1 knockdown suppressed OS cell proliferation and metastasis in vitro and in vivo.
- SNHG1 acted as a competing endogenous RNA (ceRNA) for miR-326, leading to increased NOB1 expression and promoting OS progression.
Conclusions:
- The SNHG1/miR-326/NOB1 axis plays a critical role in osteosarcoma progression.
- SNHG1 promotes OS by sponging miR-326 and upregulating the oncogene NOB1.
- SNHG1 and miR-326 show potential as diagnostic biomarkers and therapeutic targets for osteosarcoma.
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