Diltiazem potentiation of doxorubicin cytotoxicity and cellular uptake in human breast cancer cells

被引:4
作者
Al-malky, Hamdan S. [1 ]
Damanhouri, Zoheir A. [1 ]
Al Aama, Jumana Y. [2 ]
Al Qahtani, Ali A. [1 ]
Ramadan, Wafaa S. [1 ,3 ]
AlKreathy, Huda M. [1 ]
Al Harthi, Sameer E. [1 ]
Osman, Abdel-Moneim M. [1 ,4 ]
机构
[1] King Abdulaziz Univ, Fac Med, Dept Pharmacol, Jeddah, Saudi Arabia
[2] King Abdulaziz Univ, Fac Med, Dept Genet, Jeddah, Saudi Arabia
[3] Ain Shams Univ, Fac Med, Dept Anat, Cairo, Egypt
[4] Cairo Univ, Pharmacol Unit, NCI, Cairo, Egypt
关键词
activity enhancement; diltiazem; doxorubicin; MCF-7; cells; multidrug resistance; P-GLYCOPROTEIN; INHIBITION; RESISTANCE; DOCETAXEL; EXPRESSION; MECHANISM; APOPTOSIS; EFFICACY; GROWTH; DEATH;
D O I
10.2217/bmt-2019-0018
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Aim: Breast cancer is the most common cancer among Arab women and also around the world. Chronic cardiotoxicity and multidrug resistance are potential limiting factors of doxorubicin (DOX), a known anthracycline antibiotic. Materials & methods: DOX cytotoxicity was evaluated by the sulforhodamine method. DOX cellular uptake, detection of P-glycoprotein activity and the photomicrograph of MCF-7 cells were also determined. Results: Diltiazem (DIL) treatment improved DOX cytotoxic activity and increased the cellular uptake of DOX significantly and aggregation of rhodamine 123, reflecting inhibition of P-glycoprotein pump. Cytopathological investigation of MCF-7 cells revealed marked cytotoxic activity of DOX in the presence of DIL. Conclusion: DIL treatment enhanced DOX cytotoxic effect and reduced multidrug resistance, which increased the drug accumulation intracellularly.
引用
收藏
页数:10
相关论文
共 31 条
[1]   Modulation of doxorubicin-induced expression of the multidrug resistance gene in breast cancer cells by diltiazem and protection against cardiotoxicity in experimental animals [J].
Al-malky, Hamdan S. ;
Osman, Abdel-Moneim M. ;
Damanhouri, Zoheir A. ;
Alkreathy, Huda M. ;
Al Aama, Jumana Y. ;
Ramadan, Wafaa S. ;
Al Qahtani, Ali A. ;
Al Mahdi, Hadiah B. .
CANCER CELL INTERNATIONAL, 2019, 19 (1)
[2]   DILTIAZEM POTENTIATION OF DOXORUBICIN CYTOTOXICITY AND CELLULAR UPTAKE IN EHRLICH ASCITES-CARCINOMA CELLS [J].
ALSHABANAH, OA ;
OSMAN, AMM ;
ALHARBI, MM ;
ALBEKAIRI, AM ;
ALGHARABLY, NM ;
AZIZ, SA .
CHEMOTHERAPY, 1995, 41 (05) :368-377
[3]   P-glycoprotein Inhibition for Optimal Drug Delivery [J].
Amin, Md. Lutful .
DRUG TARGET INSIGHTS, 2013, 7 :27-34
[4]  
CHIN KV, 1990, CELL GROWTH DIFFER, V1, P361
[5]   L-type calcium channel blockers reverse docetaxel and vincristine-induced multidrug resistance independent of ABCB1 expression in human lung cancer cell lines [J].
Chiu, Ling-Yen ;
Ko, Jiunn-Liang ;
Lee, Yi-Ju ;
Yang, Tsung-Ying ;
Tee, Yi-Torng ;
Sheu, Gwo-Tarng .
TOXICOLOGY LETTERS, 2010, 192 (03) :408-418
[6]   Chloroquine inhibits cell growth and induces cell death in A549 lung cancer cells [J].
Fan, CD ;
Wang, WW ;
Zhao, BX ;
Zhang, SL ;
Miao, JY .
BIOORGANIC & MEDICINAL CHEMISTRY, 2006, 14 (09) :3218-3222
[7]   Inhibition of Survivin Restores the Sensitivity of Breast Cancer Cells to Docetaxel and Vinblastine [J].
Ghanbari, Parisa ;
Mohseni, Mahsa ;
Tabasinezhad, Maryam ;
Yousefi, Bahman ;
Saei, Amir Ata ;
Sharifi, Simin ;
Rashidi, Mohammad Reza ;
Samadi, Nasser .
APPLIED BIOCHEMISTRY AND BIOTECHNOLOGY, 2014, 174 (02) :667-681
[8]   The Role of Multidrug Resistance Efflux Pumps in Cancer: Revisiting a JNCI Publication Exploring Expression of the MDR1 (P-glycoprotein) Gene [J].
Gottesman, Michael M. ;
Pastan, Ira H. .
JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE, 2015, 107 (09)
[9]   Apoptosis and cell cycle arrest of human colorectal cancer cell line HT-29 induced by vanillin [J].
Ho, KetLi ;
Yazan, Latifah Saiful ;
Ismail, Norsharina ;
Ismail, Maznah .
CANCER EPIDEMIOLOGY, 2009, 33 (02) :155-160
[10]   Blockade of L-type Ca2+ channel attenuates doxorubicin-induced cardiomyopathy via suppression of CaMKII-NF-κB pathway [J].
Ikeda, Soichiro ;
Matsushima, Shouji ;
Okabe, Kosuke ;
Ikeda, Masataka ;
Ishikita, Akihito ;
Tadokoro, Tomonori ;
Enzan, Nobuyuki ;
Yamamoto, Taishi ;
Sada, Masashi ;
Deguchi, Hiroko ;
Morimoto, Sachio ;
Ide, Tomomi ;
Tsutsui, Hiroyuki .
SCIENTIFIC REPORTS, 2019, 9 (1)