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العنوان
Effect of Yttrium oxide Nanoparticles on breast cancer cell lines with different metastatic potential /
المؤلف
Basant Emad Sayed Hoseny,
هيئة الاعداد
باحث / Basant Emad Sayed Hoseny
مشرف / Ismail Abdelshafy Abdelhamid
مشرف / Sherif Abdel-Aziz Ibrahim
مشرف / Hanan Ramadan Mohamed
مناقش / Ahmed Said Alazzouni
الموضوع
Biotechnology
تاريخ النشر
2022.
عدد الصفحات
60 p. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
Chemistry (miscellaneous)
تاريخ الإجازة
25/6/2022
مكان الإجازة
جامعة القاهرة - كلية العلوم - Chemistry
الفهرس
Only 14 pages are availabe for public view

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from 116

Abstract

The number of new cancer cases is increasing at an alarming rate around the world. Breast cancer is the most frequent malignancy among women all around the world with over 1 million new cases each year. Yttrium oxide (Y2O3) is a rare earth metal oxide with strong antioxidant action. Y2O3 nanoparticles (Y2O3 NPs) are used in a number of different applications, including biological imaging, the material sciences, and in the chemical synthesis of inorganic compounds. The current study was conducted to evaluate the anticancer activity of Y2O3 NPs. On a cell line of human breast cancer MDA-MB-231. Cell viability, oxidative stress, DNA damage, and mRNA expression levels of apoptosis-related genes (p53, BAX, Bcl-2, and casp8) were evaluated in MDA-MB-231 cells using X-ray diffraction (XRD), Size distribution, Zeta potential, and transmission electron microscopy (TEM). Cells subjected to Y2O3 NPs treatment. MTT assay revealed the cytotoxic potential of Y2O3 NPs with an IC50 of 74.4 µg/mL against MDA-MB-231 cells. Interestingly, Y2O3 NPs had a subtle cytotoxic effect against the normal retina cell line RPE1. Moreover, treatment with Y2O3 NPs resulted in increased reactive oxygen species (ROS)-induced DNA damage evidenced by comet assay. Mechanistically, Y2O3 NPs significantly down-regulated Bcl-2 gene expression level. In conclusion, Y2O3 NPs have the potential to exert an anticancer activity against breast cancer possibly via increased ROS and the subsequent DNA damage leading to apoptosis.