scholarly journals Multidrug resistant P-glycoprotein positive L1210/VCR cells are also cross-resistant to cisplatin via a mechanism distinct from P-glycoprotein-mediated drug efflux activity

2009 ◽  
Vol 28 (4) ◽  
pp. 391-403 ◽  
Author(s):  
L. Gibalová ◽  
J. Sedlák ◽  
M. Labudová ◽  
M. Barančík ◽  
A. Reháková ◽  
...  
1996 ◽  
Vol 48 (5) ◽  
pp. 522-525 ◽  
Author(s):  
KEN-ICHI MIYAMOTO ◽  
KEIKO KOGA-TAKEDA ◽  
KENJIRO KOGA ◽  
TAEYUKI OHSHIMA ◽  
MASAAKI NOMURA

Author(s):  
Runze Zhao ◽  
Xiaoyue Ning ◽  
Mengqi Wang ◽  
Ao Yu ◽  
Yongjian Wang

Despite the excellent progress of chemotherapy and phototherapy in tumor treatment, their effectiveness on multidrug-resistant tumors (MDR) is still unsatisfactory. One of the main obstacles is drug efflux caused by...


2018 ◽  
Vol 10 (1) ◽  
pp. 102
Author(s):  
Robby Hertanto ◽  
Wilson Bastian ◽  
Paramita . ◽  
Melva Louisa

Objective: The aim of the present study was to determine whether curcumin (CM) can prevent drug sensitivity of breast cancer (BC) cells when E andβ-E2 are administered together and whether the underlying mechanism involves modulation of drug efflux transporters.Methods: MCF7 BC cells were treated with the vehicle only, E+β-E2, or E+β-E2+CM repeatedly for 8 weeks. Afterward, the cells were harvested,counted, and isolated for total RNA extraction. Total RNA was then processed into cDNA and further processed for the determination of mRNAexpression patterns of drug efflux transporters (P-glycoprotein, BCRP, and MRP1).Results: Decreased sensitivity of BC cells was shown by the increased cell viability of MCF7 cells after 8 weeks. This condition was accompanied withincreased mRNA expression of P-glycoprotein, BCRP, and MRP1 in cells treated with E+β-E2, as compared with the vehicle only. CM, administered incombination with E+β-E2, resulted in decreased cell viability versus E and β-E2 and also decreased in mRNA expression of P-glycoprotein, BCRP, andMRP1.Conclusion: CM partially reversed the sensitivity loss of BC cells to E in the presence of β-E2 by modulating drug efflux transporters.


2012 ◽  
Vol 32 (6) ◽  
pp. 559-566 ◽  
Author(s):  
Yan Xu ◽  
Feng Zhi ◽  
Guangming Xu ◽  
Xiaolei Tang ◽  
Sheng Lu ◽  
...  

MDR (multidrug-resistance) represents a major obstacle to successful cancer chemotherapy and is usually accomplished by overexpression of P-gp (P-glycoprotein). Much effort has been devoted to developing P-gp inhibitors to modulate MDR. However, none of the inhibitors on the market have been successful. 1416 [1-(2,6-dimethylphenoxy)-2-(3,4-dimethoxyphenylethylamino)propane hydrochloride (phenoprolamine hydrochloride)] is a new VER (verapamil) analogue with a higher IC50 for blocking calcium channel currents than VER. In the present paper, we examined the inhibition effect of 1416 on P-gp both in vitro and in vivo. 1416 significantly enhanced cytotoxicity of VBL (vinblastine) in P-gp-overexpressed human multidrug-resistant K562/ADM (adriamycin) and KBV cells, but had no such effect on the parent K562 and KB cells. The MDR-modulating function of 1416 was further confirmed by increasing intracellular Rh123 (rhodanmine123) content in MDR cells. Human K562/ADM xenograft-nude mice model verified that 1416 potentiates the antitumour activity of VBL in vivo. RT-PCR (reverse transcriptase-PCR) and FACS analysis demonstrated that the expression of MDR1/P-gp was not affected by 1416 treatment. All these observations suggest that 1416 could be a promising agent for overcoming MDR in cancer chemotherapy.


2008 ◽  
Vol 24 (3) ◽  
pp. 290-300 ◽  
Author(s):  
Srinivasan Senthilkumari ◽  
Thirumurthy Velpandian ◽  
Nihar R. Biswas ◽  
Narayanan Sonali ◽  
Supriyo Ghose

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