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e-Poster Display Session

65P - The new mouse anti-nNav1.5 monoclonal antibody

Date

22 Nov 2020

Session

e-Poster Display Session

Topics

Basic Science

Tumour Site

Presenters

Nur Aishah Sharudin

Citation

Annals of Oncology (2020) 31 (suppl_6): S1257-S1269. 10.1016/annonc/annonc353

Authors

N.A. Sharudin, N.F.A. Che Wahab, N.S. Yaacob, N. Mohd Nor, A.A. Dominguez, M.E. Sarmiento, N.F. Mokhtar

Author affiliations

  • Institute For Research In Molecular Medicine, HUSM - Hospital Universiti Sains Malaysia, 16150 - Kubang Kerian/MY

Resources

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Abstract 65P

Background

Neonatal Nav1.5 (nNav1.5) is a potent tumour metastatic marker found re-expressed in human breast cancer cells with aggressive phenotype and breast tumour tissue positive for lymph node metastasis. Mouse anti-nNav1.5 monoclonal antibody, 4H8 was recently obtained.Neonatal Nav1.5 (nNav1.5) is a potent tumour metastatic marker found re-expressed in human breast cancer cells with aggressive phenotype and breast tumour tissue positive for lymph node metastasis. Mouse anti-nNav1.5 monoclonal antibody, 4H8 was recently obtained. This study aimed to assess the specificity of the 4H8 against nNav1.5.

Methods

4H8 was used as primary antibody in Western blot and immunocytochemistry tested on cells and cell lysates, respectively of two human breast cancer cell line; MDA-MB-231+nNav1.5 and MCF-7-nNav1.5, a mouse mammary cancer cell line, 4T1+nNav1.5, a non-cancerous human breast epithelial, MCF-10A-nNav1.5 and tumour tissue lysate from an orthotopic syngeneic mouse model (4T1+nNav1.5/BALB/c).

Results

were consistent with nNav1.5 protein being more abundantly expressed in aggressive human breast cancer cell line, MDA-MB-231+nNav1.5 and mouse mammary cancer cell line, 4T1+nNav1.5 and tumour tissue lysate from an orthotopic syngeneic mouse model (4T1+nNav1.5/BALB/c) as compared to MCF-7-nNav1.5 and MCF-10A-nNav1.5.

Conclusions

The new antibody described in this work can be a novel tool in studying nNav1.5 expression in breast cancer.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

Institute of Research for Molecular Medicine.

Funding

Has not received any funding.

Disclosure

All authors have declared no conflicts of interest.

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