Irfan Irsyad bin Azahar

I am highly interested in doing research and collecting data, having positive attitude, versatile, independent yet highly inquisitive. I also have a talent of tutoring and mentoring and having good management skills.

EDUCATION

Master of Science in Molecular Medicine Institute for Research in Molecular Medicine (INFORM), Univer Sains Malaysia Glutamate Regulation of Voltage-Gated Sodium Channels (VGSCs) in Breast Cancer Cell Lines of Different Metastatic PotentialBachelor of Science (Honours) Biology School of Applied Science, Universiti Teknologi MARAAntioxidant, Toxicity and Proximate Analysis of Parkia Speciosa (Petai) CGPA: 3.49 Matriculation Program (Module 3) Johor Matriculation College CGPA: 3.57 Sijil Pelajaran Malaysia (SPM) Victoria Institution, Kuala Lumpur

RESEARCH INTERESTS

Health Sciences
Molecular Biology
Public Health

Scopus Publications

Upregulation of MHC I Antigen Processing Machinery Gene Expression in Breast Cancer Cells by Trichostatin A
A. H. Murtadha, N. A. Sharudin, I. I. M. Azahar, A. T. Che Has, and N. F. Mokhtar
Pleiades Publishing Ltd



Upregulation of MHC I Antigen Processing Machinery Gene Expression in Breast Cancer Cells by Trichostatin A




nNav1.5 expression is associated with glutamate level in breast cancer cells
Irfan Irsyad Azahar, Nur Aishah Sharudin, Ahmad Hafiz Murtadha Noor Din, Ahmad Tarmizi Che Has, Siti Norasikin Mohd Nafi, Hasnan Jaafar, and Noor Fatmawati Mokhtar
Springer Science and Business Media LLC
Abstract Background Glutamate and voltage-gated sodium channels, both have been the target of intense investigation for its involvement in carcinogenesis and progression of malignant disease. Breast cancer with increased level of glutamate often metastasize to other organs (especially bone), whilst re-expression of ‘neonatal’ Nav1.5, nNav1.5 in breast cancer is known to promote cell invasion in vitro, metastasis in vivo and positive lymph node metastasis in patients. Methods In this study, the role of nNav1.5 in regulating glutamate level in human breast cancer cells was examined using pharmacological approach (VGSCs specific blocker, TTX, glutamate release inhibitor, riluzole and siRNA-nNav1.5). Effect of these agents were evaluated based on endogenous and exogenous glutamate concentration using glutamate fluorometric assay, mRNA expression of nNav1.5 using qPCR and finally, invasion using 3D culture assay. Results Endogenous and exogenous glutamate levels were significantly higher in aggressive human breast cancer cells, MDA-MB-231 cells compared to less aggressive human breast cancer cells, MCF-7 and non-cancerous human breast epithelial cells, MCF-10A. Treatment with TTX to MDA-MB-231 cells resulted in significant reduction of endogenous and exogenous glutamate levels corresponded with significant suppression of cell invasion. Subsequently, downregulation of nNav1.5 gene was observed in TTX-treated cells. Conclusions An interesting link between nNav1.5 expression and glutamate level in aggressive breast cancer cells was detected and requires further investigation.


Invasion and Metastasis Suppression by Anti-Neonatal Nav1.5 Antibodies in Breast Cancer
Nur Sharudin, Ahmad Murtadha Noor Din, Irfan Azahar, Mawaddah Mohd Azlan, Nik Yaacob, Maria Sarmiento, Armando Dominguez, and Noor Fatmawati Mokhtar
EpiSmart Science Vector Ltd
Background: Detectable neonatal Nav1.5 (nNav1.5) expression in tumour breast tissue positive for lymph node metastasis and triple-negative subtype serves as a valid tumour-associated antigen to target and prevent breast cancer invasion and metastasis. Therapeutic antibodies against tumour antigens have become the predominant class of new drugs in cancer therapy because of their fewer adverse effects and high specificity. Objective: This study was designed to investigate the therapeutic and anti-metastatic potential of the two newly obtained anti-nNav1.5 antibodies, polyclonal anti-nNav1.5 (pAb-nNav1.5) and monoclonal anti-nNav1.5 (mAb-nNav1.5), on breast cancer invasion and metastasis. Methods: MDA-MB-231 and 4T1 cells were used as in vitro models to study the effect of pAb-nNav1.5 (59.2 µg/ml) and mAb-nNav1.5 (10 µg/ml) (24 hours treatment) on cell invasion. 4T1-induced mammary tumours in BALB/c female mice were used as an in vivo model to study the effect of a single dose of intravenous pAb-nNav1.5 (1 mg/ml) and mAb-nNav1.5 (1 mg/ml) on the occurrence of metastasis. Real-time PCR and immunofluorescence staining were conducted to assess the effect of antibody treatment on nNav1.5 mRNA and protein expression, respectively. The animals’ body weight, organs, lesions, and tumour mass were also measured and compared. Results: pAb-nNav1.5 and mAb-nNav1.5 treatments effectively suppressed the invasion of MDA-MB-231 and 4T1 cells in the 3D spheroid invasion assay. Both antibodies significantly reduced nNav1.5 gene and protein expression in these cell lines. Treatment with pAb-nNav1.5 and mAb-nNav1.5 successfully reduced mammary tumour tissue size and mass and prevented lesions in vital organs of the mammary tumour animal model whilst maintaining the animal’s healthy weight. mRNA expression of nNav1.5 in mammary tumour tissues was only reduced by mAb-nNav1.5. Conclusion: Overall, this work verifies the uniqueness of targeting nNav1.5 in breast cancer invasion and metastasis prevention, but more importantly, humanised versions of mAb-nNav1.5 may be valuable passive immunotherapeutic agents to target nNav1.5 in breast cancer.


Influence of nNav1.5 on MHC class I expression in breast cancer
Ahmad Hafiz Murtadha, Irfan Irsyad Mohd Azahar, Nur Aishah Sharudin, Ahmad Tarmizi Che Has, and Noor Fatmawati Mokhtar
Springer Science and Business Media LLC