Abstract 1383
Background
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.
Methods
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.
Results
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.
Conclusions
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.
Funding
National Natural Science Foundation of China.
Disclosure
All authors have declared no conflicts of interest.
Resources from the same session
4242 - HIV, HBV and HCV screening practices in oncology: a cross-sectional interregional survey
Presenter: Isabelle Poizot-Martin
Session: Poster Display session 1
Resources:
Abstract
1267 - Genetic landscape of KEAP1 and NFE2L2 mutated cancers from the AACR GENIE database
Presenter: Mark Zaki
Session: Poster Display session 1
Resources:
Abstract
878 - β-arrestin1 is involved in the Ras-induced malignant transformation
Presenter: Takashi Shibano
Session: Poster Display session 1
Resources:
Abstract
4143 - Incidence of second cancer among PLWHIV: retrospective observational study of a series of 601 patients in the French CANCERVIH network
Presenter: Jean-Philippe Spano
Session: Poster Display session 1
Resources:
Abstract
5145 - A challenging task – Identifying carcinoma of unknown primary (CUP) patients according to ESMO guidelines: the CUPISCO trial experience
Presenter: Chantal Pauli
Session: Poster Display session 1
Resources:
Abstract
1737 - Incidence and Outcome of chronic lymphocytic leukemia with Deletion 17p: An Indian experience; challenges and opportunities
Presenter: Ajay Gogia
Session: Poster Display session 1
Resources:
Abstract
2596 - Driving solo? Investigation into collaborating mutations in SDH-deficient neoplasia
Presenter: Jonathan Killian
Session: Poster Display session 1
Resources:
Abstract
1499 - The potential of a novel antiangiogenic VEGFR1-D2 binding peptide in oncology therapeutics
Presenter: Afsaneh Sadre Momtaz
Session: Poster Display session 1
Resources:
Abstract
1775 - First-in-human phase I study of TAS-117, an allosteric AKT inhibitor, in patients with advanced solid tumors
Presenter: Mayu Yunokawa
Session: Poster Display session 1
Resources:
Abstract
4584 - First-in-human study of ABBV-621 in patients (pts) with previously treated sold tumors: Dose-optimization cohorts
Presenter: Emiliano Calvo
Session: Poster Display session 1
Resources:
Abstract