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Updated: Jan 14, 2026

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells
Published on: April 7, 2017
Kaempferol regulates Ewing sarcoma progression via miR-26b-5p-mediated expression of the family with sequence
Yiquan Ji1, Tian Gao1, Zehua Xu1
1Department of Orthopaedics, The Second Hospital of Jiaxing, No. 1518, Huancheng Road Nanhu District, Jiaxing, Zhejiang Province, 314000, P.R. China.
Abstract:
Ewing sarcoma (ES) is a highly aggressive pediatric bone cancer with limited treatment options for metastatic or recurrent cases. This study investigated the antitumor effects of kaempferol, a natural flavonoid, on ES and its underlying molecular mechanisms. In vitro experiments demonstrated that kaempferol significantly inhibited the proliferation, migration, and invasion of SK-ES-1 cells in a dose- and time-dependent manner. Mechanistically, kaempferol upregulated miR-26b-5p, which directly targeted and suppressed FAM98A, a pro-oncogenic protein. This regulation led to the inhibition of the EGFR/PI3K/AKT/NF-κB signaling pathway, reducing tumor growth and metastasis. In vivo studies further confirmed that kaempferol suppressed ES tumor growth in a xenograft mouse model, while miR-26b-5p knockdown partially reversed this effect. Our findings suggest that kaempferol exerts its antitumor activity in ES by modulating the miR-26b-5p/FAM98A axis and downstream signaling pathways, highlighting its potential as a novel therapeutic agent for ES treatment.
Insights
Kaempferol, a natural flavonoid, effectively inhibits Ewing sarcoma (ES) progression by upregulating miR-26b-5p, suppressing FAM98A, and blocking key cancer pathways. This natural compound shows promise for treating this aggressive pediatric bone cancer.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Ewing sarcoma (ES) is an aggressive pediatric bone cancer with poor prognosis for metastatic or recurrent disease.
- Current treatment options for advanced ES are limited, necessitating the exploration of novel therapeutic strategies.
Purpose of the Study:
- To investigate the antitumor effects of kaempferol, a natural flavonoid, on Ewing sarcoma.
- To elucidate the molecular mechanisms underlying kaempferol's anti-ES activity.
Main Methods:
- In vitro studies using SK-ES-1 cells to assess proliferation, migration, and invasion.
- Molecular analysis including miR-26b-5p and FAM98A expression, and Western blotting for signaling pathway components.
- In vivo xenograft mouse model to evaluate kaempferol's efficacy on tumor growth.
Main Results:
- Kaempferol significantly inhibited ES cell proliferation, migration, and invasion in a dose- and time-dependent manner.
- Kaempferol upregulated miR-26b-5p, which suppressed FAM98A expression, leading to inhibition of the EGFR/PI3K/AKT/NF-κB pathway.
- Kaempferol suppressed tumor growth in vivo, an effect partially reversed by miR-26b-5p knockdown.
Conclusions:
- Kaempferol demonstrates significant antitumor effects against Ewing sarcoma.
- The mechanism involves modulation of the miR-26b-5p/FAM98A axis and downstream signaling pathways.
- Kaempferol represents a potential novel therapeutic agent for Ewing sarcoma treatment.
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