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Updated: Nov 1, 2025

Author Spotlight: RNA FISH for Locating lncRNA-SNHG6 in Osteosarcoma Cells
Published on: June 16, 2023
Long non-coding RNA X-inactive specific transcript promotes osteosarcoma metastasis via modulating microRNA-758/Rab16
Wei Liu1, Qiuping Long1, Li Zhang1
1Department of Orthopedics Trauma, Nanhua Hospital Affiliated to Nanhua University, Hengyang, China.
Background:
As a common malignant bone sarcoma, osteosarcoma (OS) affects the health and lives of many people. Here, we probed the effects of long non-coding RNA (lncRNA) X-inactive specific transcript (XIST) and microRNA-758 (miR-758) on OS metastasis, and examined possible downstream effector.
Methods:
Quantitative reverse transcription PCR (qRT-PCR) was performed to detect the expressions of XIST and miR-758 in OS tissues and cells. Cell transfection was carried out to alter the levels of XIST and miR-758 in OS cells, and cell viability, migration, and invasion were assessed. Subsequently, qRT-PCR and a dual-luciferase reporter assay were conducted to analyze the regulatory effects of XIST on miR-758 and miR-758 on Rab16. Finally, we investigated whether Rab16 was the downstream effector of XIST/miR-758 axis.
Results:
XIST was highly expressed in OS tissues and cells, but the opposite was seen for miR-758. In OS cells, migration, invasion, and epithelial-mesenchymal transformation (EMT) was promoted by overexpression of XIST and miR-758 inhibitor, but were inhibited by XIST knockdown and miR-758 mimics. XIST regulated miR-758 expression, and miR-758 regulated Rab16 expression in OS cells. Overexpression of Rab16 reversed the effects of miR-758 mimics on OS cell migration and invasion.
Conclusions:
XIST contributed to OS cell migration, invasion, and EMT via regulation of miR-758/Rab16.
Insights
Long non-coding RNA XIST promotes osteosarcoma metastasis by regulating microRNA-758 and Rab16. This study reveals a novel mechanism driving cancer spread in bone sarcoma.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Osteosarcoma (OS) is a prevalent bone sarcoma impacting numerous lives.
- Understanding the molecular mechanisms of OS metastasis is crucial for effective treatment.
Purpose of the Study:
- To investigate the roles of long non-coding RNA XIST and microRNA-758 in osteosarcoma metastasis.
- To identify the downstream effector of the XIST/miR-758 axis in OS.
Main Methods:
- Quantitative reverse transcription PCR (qRT-PCR) to assess XIST and miR-758 expression.
- Cell transfection to manipulate XIST and miR-758 levels, followed by assays for cell viability, migration, and invasion.
- Dual-luciferase reporter assay to confirm regulatory interactions between XIST, miR-758, and Rab16.
Main Results:
- XIST was upregulated, while miR-758 was downregulated in OS tissues and cells.
- XIST overexpression and miR-758 inhibition promoted OS cell migration, invasion, and epithelial-mesenchymal transition (EMT).
- XIST directly regulated miR-758, which in turn regulated Rab16; Rab16 overexpression counteracted miR-758 mimic effects.
Conclusions:
- The lncRNA XIST facilitates osteosarcoma cell migration, invasion, and EMT.
- XIST exerts its pro-metastatic effects through the miR-758/Rab16 signaling pathway.
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