Siti Zainab Salim1*, Shahrul Bariyah Sahul Hamid2, Seoparjoo Azmel Mohd Isa2, Tengku Rogayah Tengku Abdul Rashid1
1. Electron Microscopy Unit, Special Resource Centre, Institute for Medical Research, National Institute of Health, Ministry of Health, 40170 Setia Alam, Selangor
2. Biomedical Science Department, Advance Medical and Dental Institute, Universiti Sains Malaysia, 13200 Kepala Batas, Pulau Pinang
*Corresponding author: Siti Zainab Salim.
ABSTRACT
INTRODUCTION: Dyslipidaemia is commonly associated with elevated low-density lipoprotein (LDL) cholesterol, very low-density lipoprotein (VLDL) cholesterol, and triglycerides. Altered lipid profiles may enhance HER2 breast cancer stability and function, thus reducing the effectiveness of treatment. Thus, the molecular mechanisms need to be investigated further.
OBJECTIVE(S): This study aimed to determine the effect of oxLDL and VLDL in relation to drug-resistant HER2-positive breast cancer cell lines.
MATERIALS & METHODS: HER2 breast cancer resistant cells were exposed to oxLDL and VLDL for 72 hours. Cell viability was measured and morphological changes were identified using a phase contrast microscope. Flow cytometry analysis was done for the measurement of viability and apoptotic cells.
RESULTS: Cellular morphological changes showed cells treated with oxLDL were spherical, whereas cells exposed to VLDL had a fibroblast-like appearance. Cell viability was studied using the cell proliferation assay. Resistant cells exposed to oxLDL had a higher IC50 value (73.8 µg/mL) than the parent cells (30.9 µg/mL). Meanwhile, exposure to VLDL did not inhibit the growth factor, where the IC50 was not achieved. For cell death, the expression of 7AAD showed that the resistant cells exposed to 10 µg/ml oxLDL had the highest percentage of cell death compared to the resistant cells exposed to VLDL.
CONCLUSION: This study showed the effect of lipoproteins in resistant HER2-positive breast cancer cell lines. It was suggested that VLDL caused significant morphological changes and increased cell viability in HER2 resistant and parent cells, while oxLDL inhibited cell growth at different concentrations.
KEYWORDS: Breast Cancer, Molecular Biology, Lipoproteins


