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Volume 2

Journal of Molecular Cancer

Cancer & Primary Healthcare 2019

May 20-21, 2019

Cancer Research & Oncology

Primary Healthcare and Medicare Summit

May 20-21, 2019 | Rome, Italy

25

th

Global Meet on

World Congress on

&

The Notch ligand DLL1 exerts pro-carcinogenic effects in human breast cancer luminal

AMCF-7 cells

Gabriela Silva

iBET - Instituto de Biologia Experimental e Tecnológica, Portugal

Background:

Breast cancer (BC) is the most common cancer in women and has a high rate of relapse and

death. The Notch signaling pathway plays an important role in normal breast development and homeostasis.

Dysregulation of Notch receptors and its ligands Jagged1, Jagged2, and DLL4 has been detected in BC and

implicated in tumor development, progression, drug resistance, and recurrence. The Notch ligand DLL1 has

emerged as a player in BC as its expression is undetectable in normal breast tissues, but moderate to high in

BC. In this study, we examined the role of DLL1 in BC luminal A MCF-7 cells. Methodology: DLL1 siRNA

and recombinant DLL1 protein were used to evaluate the effects of DLL1 in MCF-7 cells. Gene expression

was analyzed by qRT-PCR and immunobloting. Cell growth and proliferation were assessed by trypan blue

exclusion and the MTT methods. Microscopy and scratch wound-healing assays were used to evaluate colony

formation and cell migration. Findings: In MCF-7 cells, DLL1 downregulation reduced proliferation, colony

formation efficiency, and migration. On the other hand, treatment with recombinant DLL1, which activates

the Notch signaling pathway, increased MCF-7 cell proliferation and migration, confirming that DLL1

contributes to these processes in these luminal A BC cells. Conclusion: These findings provide evidence that

DLL1 contributes to the pro-carcinogenic effects of luminal A MCF-7 cells by promoting clonogenic growth,

cell proliferation, and migration.

Biography

Gabriela Silva holds a PhD in Biology from the Instituto de Biologia Experimental e Tecnológica, Portugal. From 2002 to 2008 she

worked as Post-Doctoral fellow in the Instituto Gulbenkian de Ciência, Portugal, on projects that contributed to the understanding how

HO1-1 protein affords cytoprotective and anti-inflammatory effects in various diseases. After that, she developed research in cancer.

First on the role of HDAC inhibitors on hematologic malignancies and then on the mechanisms by which p16 protein exerts anti-

oncogenic effects in osteosarcoma and on the mechanisms underlying the stromal fibroblast transformation in breast cancer. Since

2014, she has been a scientist at Instituto de Biologia Experimental e Tecnológica, Portugal, where she works on projects in the fields

of biopharmaceutical process development and oncology. Her main scientific interests relate to the mechanisms underlying cancer

development and therapy.

gabrielasilva@ibet.pt

J Mol Cancer, Volume 2