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Poster Display session 1

1383 - let-7a suppress Ewing sarcoma CSCs' malignant phenotype through forms a positive feedback regulation loop with lin28 via STAT3


28 Sep 2019


Poster Display session 1


Tumour Site



Xu Jiang


Annals of Oncology (2019) 30 (suppl_5): v683-v709. 10.1093/annonc/mdz283


X. Jiang, X. jiang

Author affiliations

  • Spine Center, 2nd Affiliated Hospital of Nanchang University, 330006 - Nanchang/CN


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Abstract 1383


Ewing’s sarcoma (ES) is a highly malignant primary bone tumor, and ewing’s sarcoma stem cells (CSCs) are the main cause of tumor recurrence and metastasis. This paper will further discuss the mechanism of let-7a in the development and progression of ewing’s sarcoma CSCs, laying an experimental basis and theoretical basis for the biological treatment of ewing’s sarcoma.


In this study, we intend to isolate CSCs from ES cells cultured in vitro by side group cell sorting and flow cytometry, and then detect the effect of let-7a on the malignant phenotype of ewing’s sarcoma CSCs, and further verify the regulatory role of let-7a in ewing’s sarcoma CSCs in vitro and in vivo experiments.


We successfully isolated Ewing sarcoma cancer stem cells(CSCs) by side population cells (SP) sorting method. The immunohistochemical results showed that STAT3 was highly expressed in ES tissues and negatively correlated with let-7a.Overexpression of the let - 7a can suppress the malignant phenotype of Ewing sarcoma CSCs, and inhibited the growth of subcutaneous xenograft tumor of ewing’s sarcoma CSCs.Bioinformatics analysis found that singal transducer and activator of transcription 3 (STAT3) is a direct target gene of let - 7a, STAT3 and its downstream factor lin28 form a positive feedback loop with let-7a, participate in Ewing sarcoma CSCs function regulation.


let-7a suppress Ewing sarcoma CSCs’ malignant phenotype through forms a positive feedback regulation loop with lin28 via STAT3.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

The second affiliated Hospital of Nanchang University.


National Natural Science Foundation of China.


All authors have declared no conflicts of interest.

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