Oops, you're using an old version of your browser so some of the features on this page may not be displaying properly.

MINIMAL Requirements: Google Chrome 24+Mozilla Firefox 20+Internet Explorer 11Opera 15–18Apple Safari 7SeaMonkey 2.15-2.23

Cocktail & Poster Display session

49P - MiR-155 promotes breast cancer progression by upregulating cancer stemness

Date

04 Oct 2023

Session

Cocktail & Poster Display session

Presenters

Jeonghee Han

Citation

Annals of Oncology (2023) 8 (suppl_1_S5): 1-55. 10.1016/esmoop/esmoop101646

Authors

J. Han

Author affiliations

  • Surgery, CHA Bundang Medical Center, 13496 - Seongnam/KR

Resources

This content is available to ESMO members and event participants.

Abstract 49P

Background

To date, miR-155 is known as an oncogenic miRNA with a well-documented role in breast cancer. Cancer stemness plays an important role in various aspects of carcinogenesis. The aim of this study is to investigate the effect of miR-155 on breast cancer proliferation by upregulating cancer stem cells.

Methods

In vivo-tumor growth and metastasis were measured across polyomavirus middle T antigen (PyVmT) transgenic mice and PyVmT miR-155 knockout mice. Western blot and quantitative real-time polymerase chain reaction (qRT-PCR) were employed to determine the protein and mRNA levels, respectively. The cancer stemness was assessed by sphere formation as well as the expression of the related markers. The miR-155 target genes were predicted and analyzed by western blot and luciferase assay.

Results

Upregulation of miR-155 in breast cancer tissues of mice identified poor prognosis and cancer metastasis. Upregulation of miR-155 was also found in breast cancer stem cells. Ectopic expression of miR-155 promotes the stemness of breast cancer cells. Conversely, depletion of miR-155 attenuates the stemness of these cells. miR-155 directly binds to CYLD and Sharp-1 to influence breast cancer stemness.

Conclusions

MicroRNA-155 promotes breast cancer progression by upregulating breast cancer stemness.

Editorial acknowledgement

Clinical trial identification

Legal entity responsible for the study

The author.

Funding

Has not received any funding.

Disclosure

The author has declared no conflicts of interest.

This site uses cookies. Some of these cookies are essential, while others help us improve your experience by providing insights into how the site is being used.

For more detailed information on the cookies we use, please check our Privacy Policy.

Customise settings
  • Necessary cookies enable core functionality. The website cannot function properly without these cookies, and you can only disable them by changing your browser preferences.