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Related Experiment Video

Updated: May 12, 2026

Cytotoxic Efficacy of Photodynamic Therapy in Osteosarcoma Cells In Vitro

Cytotoxic Efficacy of Photodynamic Therapy in Osteosarcoma Cells In Vitro

Published on: March 18, 2014

Rotenone Inhibited Osteosarcoma Cell Growth Through USP47-Induced Decreases in FEN1 Stability and DNA Integrity.

Zhen Li¹, Xiang Ma², Hengwei Ma³

¹Department of Medical Oncology, The Second Affiliated Hospital of Xuzhou Medical University, Xuzhou, 221000, People's Republic of China.

Drug Design, Development and Therapy

|May 11, 2026

Summary

Rotenone targets USP47, decreasing FEN1 stability and DNA integrity, thereby inhibiting osteosarcoma (OS) growth. This study identifies rotenone as a potential therapeutic agent for OS by elucidating its anti-OS mechanisms.

Keywords:

DNA damage FEN1 USP47 osteosarcoma rotenone

Related Experiment Videos

Last Updated: May 12, 2026

Cytotoxic Efficacy of Photodynamic Therapy in Osteosarcoma Cells In Vitro

Cytotoxic Efficacy of Photodynamic Therapy in Osteosarcoma Cells In Vitro

Published on: March 18, 2014

Area of Science:

Oncology
Molecular Biology
Biochemistry

Background:

Osteosarcoma (OS) is a common pediatric bone cancer.
Previous research indicated rotenone inhibits OS metastasis.
The impact of rotenone on OS cell growth and its mechanisms were previously unknown.

Purpose of the Study:

To investigate rotenone's role in osteosarcoma (OS) progression.
To identify the direct molecular target of rotenone in OS.
To elucidate the mechanisms underlying rotenone's effects on OS cells.

Main Methods:

Utilized molecular docking and Biacore assays to confirm rotenone-USP47 interaction.
Employed co-immunoprecipitation, immunofluorescence, and cycloheximide assays to study USP47-FEN1 relationship.
Assessed cell cycle, apoptosis, DNA damage, and ubiquitination status via flow cytometry, comet assays, and deubiquitination assays.
Validated findings in vivo using immunohistochemistry and a xenograft mouse model.

Main Results:

Knockdown of FEN1 and USP47 induced cell cycle arrest and apoptosis via DNA damage in OS cells.
FEN1 directly interacts with USP47, which regulates FEN1 stability through deubiquitination.
Rotenone physically interacts with USP47, modulating its expression and ubiquitination, leading to decreased FEN1 stability and DNA integrity.
In vivo xenograft studies confirmed rotenone's anti-OS activity.

Conclusions:

Rotenone directly targets USP47 in osteosarcoma (OS).
Rotenone reduces FEN1 protein stability and compromises DNA integrity.
Rotenone demonstrates potential as a therapeutic agent for OS.