فهرس بحوث جامعة سومر: Glucose Deprivation Induced By Acarbose And Oncolytic Newcastle Disease Virus Promote Metabolic Oxidative Stress And Cell Death In A Breast Cancer Model

عرض تفاصيل البحث

ادناه جميع التفاصيل الخاصة بالبحث المطلوب عرضه. توفر هذه المنصة معلومات اساسية حول البحث, لمزيد من التفاصيل يرجى متابعة التصفح من خلال الضغط على الرابط الاصلي للبحث او رابط DOI.

عنوان البحث

Glucose Deprivation Induced By Acarbose And Oncolytic Newcastle Disease Virus Promote Metabolic Oxidative Stress And Cell Death In A Breast Cancer Model

عنوان المجلة

Front. Mol. Biosci

ISSN-2296-889X

تفاصيل النشر

سنة النشر - 2022 / الفهرس الاصلي للمجلة - 9 : 1 (عدد الصفحات 10)

تصنيف البحث

Biochemistry and physiology - المجموعة الطبية

رابط DOI

https://doi.org/10.3389/fmolb.2022.816510

رابط البحث

فتح في موقع المجلة الرسمي

البحث والاستدامة

غير مرتبط باهداف التنمية المستدامة

البحث والمجتمع

نعم , يدعم

الكلمات المفتاحية

glucose deprivation, oncolytic virotherapy, oxidative stress, apoptosis, cancer

اسم الباحث	جهة الانتساب	بلد الباحث
Qayssar Abdul Hussein Obaid	University of Sumer	Iraq
Khalisa Khudair	University of Baghdad	Iraq
Ahmed Majeed Alshammari	University of Mustansiriyah	Iraq

Cancer cells are distinguished by enhanced glucose uptake and an aerobic glycolysis pathway in which its products support metabolic demands for cancer cell growth and proliferation. Inhibition of aerobic glycolysis is a smart therapeutic approach to target the progression of the cancer cell. We employed acarbose (ACA), a particular alphaglucosidase inhibitor, to induce glucose deprivation combined with oncolytic Newcastle disease virus (NDV) to enhance antitumor activity. In this work, we used a mouse model of breast cancer with mammary adenocarcinoma tumor cells (AN3) that were treated with ACA, NDV, and a combination of both. The study included antitumor efficacy, relative body weight, glucose level, hexokinase (HK-1) level by ELISA, glycolysis product (pyruvate), total ATP, oxidative stress (ROS and reduced glutathione), and apoptosis by immunohistochemistry. The results showed significant antitumor efficacy against breast cancer after treatment with combination therapy. Antitumor efficacy was accompanied by a reduction in body weight and glucose level, HK-1 downregulation, inhibition of glycolysis products (pyruvate), total ATP, induction of oxidative stress (increase ROS and decrease reduced glutathione), and apoptotic cell death. The findings propose a novel anti–breast cancer combination involving the suppression of glycolysis, glucose deprivation, oxidative stress, and apoptosis, which can be translated clinically.