77P - Down-regulated miR-486-5p acts as a tumor suppressor in breast cancer patients by targeting the metastatic mediator ICAM-1 (77P)

Date 08 December 2017
Event ESMO Immuno-Oncology Congress 2017
Session Lunch & Poster Display session
Topics Anti-Cancer Agents & Biologic Therapy
Cancer Immunology and Immunotherapy
Translational Research
Presenter Ramah Abdallah
Citation Annals of Oncology (2017) 28 (suppl_11): xi6-xi29. 10.1093/annonc/mdx711
Authors R. Abdallah1, R.A. Youness1, N. El Meckawy2, A.F. El Sebaei3, A. Abdelmotaal4, R.A. Assal5
  • 1Molecular Genetics Research Team, Pharmaceutical Biology Department, Faculty of Pharmacy and Biotechnology, German University in Cairo, 11835 - New Cairo/EG
  • 2Surgical Oncology And Endocrinology Department, International Medical Center, 11835 - Cairo/EG
  • 3Pathology Department, International Medical Center, 11835 - Cairo/EG
  • 4Pharmacognosy Department, Faculty of Pharmacy, Cairo University, 11835 - Cairo/EG
  • 5Molecular Genetics Research Team, Pharmacology And Toxicology Department, Faculty of Pharmacy and Biotechnology, German University in Cairo, 11835 - New Cairo/EG



Intracellular adhesion molecule-1 (ICAM-1) acts as a double-edged sword in breast cancer (BC) due to its impact on metastasis and its emerging role as a co-stimulatory ligand. The latter effect occurs by stimulating the cytotoxic players of the immune system; cytotoxic T lymphocytes and natural killer cells, to eradicate BC cells. To date, epigenetic regulation of ICAM-1 by microRNAs has never been investigated in BC. miR-486-5p expression is tumor-specific. It acts as a tumor-suppressor in liver cancer and oncomiR in colorectal cancer. However, its role in BC has been rarely investigated. Thus, this study aimed at investigating the impact of miR-486-5p on ICAM-1 in BC cells.


Tissues were collected from 17 BC patients. In-silico analysis was performed to predict a miRNA that could potentially target ICAM-1 with high scores. MDA-MB-231 and MCF-7 cells were cultured. MDA-MB-231 cells were transfected by miR-486-5p oligonucleotides using lipofection technique. Total RNA was extracted, reverse transcribed and quantified using qRT-PCR. Cellular viability and anchorage independent growth of MDA-MB-231 cells were measured using MTT and colony forming assays, respectively.


miR-486-5p targets ICAM-1 mRNA at 2 binding sites with high scores. In contrast to ICAM-1, miR-486-5p was downregulated in BC tissues compared to normal tissues. ICAM-1 showed higher expression in TNBC cell lines, MDA-MB-231, compared to hormone receptor positive, MCF-7 cells. Paradoxically, miR-486-5p was found to be downregulated in MDA-MB-231 compared to MCF-7 cells. Therefore, upon forcing miR-486-5p expression in MDA-MB-231 cells, (more than 900-fold increase), ICAM-1 levels were ectopically reduced. Furthermore, miR-486-5p led to a significant inhibition of BC cell growth and colony forming ability, while anti-miR-486-5p reversed those effects.


miR-486-5p decreases the metastatic property of ICAM-1. In addition, miR-486-5p acts as a tumor suppressor in BC. Thus, increasing the levels of the under-expressed miR-486-5p in TNBC tissues can be a possible therapeutic approach for halting BC progression. Moreover, the potent inhibition of ICAM-1 by miR-486-5p suggests that it is a possible target for BC therapy.

Clinical trial identification

Legal entity responsible for the study

Molecular Genetics Research Team




All authors have declared no conflicts of interest.