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Updated: Sep 2, 2025

Author Spotlight: RNA FISH for Locating lncRNA-SNHG6 in Osteosarcoma Cells
Published on: June 16, 2023
LncRNA STK4 antisense RNA 1 (STK4-AS1) promoted osteosarcoma by inhibiting p53 expression
Weitao Yao1, Jingyu Hou1, Guoqing Liu1
1Affiliated Tumor Hospital of Zhengzhou University, Henan Cancer Hospital, Zhengzhou, Henan, China.
Background:
LncRNA STK4 antisense RNA 1 (STK4-AS1) has been identified as a potential biomarker associated with multiple cancers. We proposed that STK4-AS1 plays a role in the proliferation of osteosarcoma by regulating the cell cycle.
Methods:
We compared the expression of STK4-AS1, p53, and p21 in osteosarcoma vs normal samples in clinical tissues and cell lines. We determined the effect of overexpression and knockdown of STK4-AS1 in p53 expressing osteosarcoma cells U2OS, p53 muted osteosarcoma cells MG63, and osteoblast cells hFOB on p53 and p21 expression and the cell viability. For U2OS and MG63, the cell cycle was analyzed and the expression of cyclin proteins was determined. We overexpressed p53 or p21 in STK4-AS1 overexpressed cells to explore the association of STK4-AS1 and p53 in U2OS.
Results:
The STK4-AS1 expression was higher and p53 and p21 expression were lower in osteosarcoma tissue and cells than in their non-cancer counterparts. The expression of STK4-AS1 was negatively correlated with the expression of p53 or p21. Knockdown of STK4-AS1 in U2OS decreased the cell viability, increased cells in the G0/G1 phase, decreased cells in the S and G2/M phase, decreased expression of cyclin A and B, increased p53 and p21, and had no effect on cyclin D and cyclin E, while overexpression of STK4-AS1 did the opposes. Overexpression of p53 or p21 recovered some changes caused by STK4-AS1 overexpression in U2OS. MG63 expressed no p53 and the expression of p21, cyclin A, and cyclin B, cell viability, and cell cycle were not affected by altered STK4-AS1 levels. In hFOB cells, the expression of p53 and p21 was decreased and the cell viability was increased when STK4-AS1 was overexpressed, but they were not affected when STK4-AS1 was knocked down.
Conclusion:
LncRNA STK4-AS1 promoted the cell cycle of osteosarcoma cells by inhibiting p53 expression.
Insights
Long non-coding RNA STK4 antisense RNA 1 (STK4-AS1) promotes osteosarcoma cell proliferation by inhibiting p53 expression, impacting cell cycle progression. This finding highlights STK4-AS1 as a potential therapeutic target for osteosarcoma.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Long non-coding RNA STK4 antisense RNA 1 (STK4-AS1) is implicated as a potential biomarker in various cancers.
- This study investigates the role of STK4-AS1 in osteosarcoma proliferation, specifically its regulation of the cell cycle.
Purpose of the Study:
- To determine the expression levels of STK4-AS1, p53, and p21 in osteosarcoma compared to normal tissues.
- To elucidate the functional role of STK4-AS1 in regulating osteosarcoma cell cycle progression and viability.
- To explore the relationship between STK4-AS1 and the p53/p21 pathway in osteosarcoma.
Main Methods:
- Comparative analysis of STK4-AS1, p53, and p21 expression in clinical osteosarcoma tissues and cell lines.
- Functional assays involving overexpression and knockdown of STK4-AS1 in osteosarcoma (U2OS, MG63) and normal osteoblast (hFOB) cell lines.
- Cell cycle analysis, cell viability assays, and Western blotting to assess protein expression (p53, p21, cyclins).
Main Results:
- STK4-AS1 expression was elevated, while p53 and p21 expression was reduced in osteosarcoma samples.
- STK4-AS1 knockdown in U2OS cells decreased viability, arrested the cell cycle at G0/G1, and increased p53/p21 levels.
- Functional effects of STK4-AS1 were dependent on p53 expression, with MG63 cells (p53-null) showing no significant changes.
Conclusions:
- LncRNA STK4-AS1 promotes osteosarcoma cell cycle progression by inhibiting p53 expression.
- STK4-AS1 acts as an oncogenic lncRNA in osteosarcoma, potentially through the p53/p21 pathway.
- Targeting STK4-AS1 may offer a novel therapeutic strategy for osteosarcoma.
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