scholarly journals Effects of Low Dose Fractional Radiation on Chemosensitivity of Gemcitabine-Resistant Human Pancreatic Cancer SW1900/GZ Cell

Author(s):  
Danni XU ◽  
Yanda LU ◽  
Fengxiang Han ◽  
Chunxiang Luo ◽  
Fen Huang ◽  
...  

Objective: To investigate whether low-dose fractionated radiation (LDFRT) could enhance gemcitabine sensitivity in drug-resistant human pancreatic cancer SW1900/GZ cell, and to further explore the underlying mechanism. Methods: Gemcitabine-resistant human pancreatic cancer SW1900 cell line (SW1900/GZ) was induced by high concentration gemcitabine intermittent shock in vitro. The cell counting kit 8 (CCK8) was used to determine SW1900/GZ cell lines. SW1900/GZ cells were divided into six groups as follows: control, LDFRT, high dose radiation (HDRT), gemcitabine (GEM), low dose fractional radiation plus gemcitabine (LDFRT+ GEM) and high dose radiation plus gemcitabine (HDRT+ GEM) groups. The rate of apoptosis was determined by flow cytometry (FCM). Protein levels of multidrug resistance gene (MDR) and multidrug resistance-related protein gene (MRP) were examined by Western blotting. Results: The results of CCK8 test showed that the half-maximal inhibitory concentration (IC50) of non-drug-resistant cell line SW1900 and drug-resistant cell line SW1990/GZ were 230.4ng/ml and 856.6ug/ml respectively. The IC50 of SW1990/GZ was 3700 times more than the former. LDFRT significantly promoted apoptosis in SW1900 cells. Moreover, in the LDFRT group, protein levels of MDR and MRP were markedly decreased. Conclusion: This study established an effective gemcitabine-resistant cell line SW1900 of human pancreatic cancer (SW1900/GZ cell line). LDFRT sensitizes resistant SW1900/GZ pancreatic cancer cell to gemcitabine through down-regulation the expression of MDR and MPR proteins.

2014 ◽  
Vol 33 (1) ◽  
pp. 383-390 ◽  
Author(s):  
CONGFEI WANG ◽  
WEIWEI ZHANG ◽  
MINGJUAN FU ◽  
AIQIN YANG ◽  
HEGUANG HUANG ◽  
...  

Pancreas ◽  
2003 ◽  
Vol 27 (3) ◽  
pp. 220-224 ◽  
Author(s):  
Akira Togawa ◽  
Hiroshi Ito ◽  
Fumio Kimura ◽  
Hiroaki Shimizu ◽  
Masayuki Ohtsuka ◽  
...  

2006 ◽  
Vol 74 (4) ◽  
pp. 160-166 ◽  
Author(s):  
Shiro Iuchi ◽  
Meytha Marsch-Moreno ◽  
Cristina Velez-DelValle ◽  
Karen Easley ◽  
Walid Kuri-Harcuch ◽  
...  

Oncogene ◽  
2000 ◽  
Vol 19 (44) ◽  
pp. 5098-5105 ◽  
Author(s):  
Caterina Cinti ◽  
Pier Paolo Claudio ◽  
Antonio De Luca ◽  
Monica Cuccurese ◽  
Candace M Howard ◽  
...  

Author(s):  
Muhammad Hasan Bashari ◽  
Fachreza Aryo Damara ◽  
Isna Nisrina Hardani ◽  
Gita Widya Pradini ◽  
Tenny Putri ◽  
...  

Cervical cancer is one of the most leading causes of women death. Currently, paclitaxel is still one of the main therapeutic regimens for cervical cancer patients. However, some patients developed to be paclitaxel-resistant. Hence, studies to find out the novel strategies to resolve this problem are important. Generating resistant cancer cell lines can be utilized as the potent tool to evaluate the efficacy of any therapeutic agent toward cancer drug-resistant problems. Current studies describing the methods to establish chemoresistance are lacking. Moreover, study in Indonesia conducting chemoresistance in cell line is limited. This study was aimed to elaborate the characteristics of HeLa cells during generation of paclitaxel-resistant cervical cancer cells. The parental HeLa cells were exposed to an escalating concentration of paclitaxel for a long time period. Subsequently, cells were divided into two groups for the evaluation of resistance characteristics. The values of inhibitory concentration 50 (IC50) and inhibitory concentration 90 (IC90) were analyzed using 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide (MTT) assay. Our data showed that the longer exposing periods of paclitaxel, the higher IC50 and IC90 values of HeLa cells are. IC90 of paclitaxel in HeLa Pac RB was increased from 69 pM, 440 pM, 2,561 pM and 10,337 pM on 0th, 1st, 2nd, 3rd and 4th months, respectively. Interestingly, the resistant cells were recovered to be paclitaxel-sensitive when they were not being continuously exposed to paclitaxel. In addition, the paclitaxel resistant cells become less sensitive against 5-FU but not doxorubicin, cisplatin and etoposide. We were able to generate cervical cancer HeLa paclitaxel-resistant cell line. These cell line could potentially be utilized for further studies in order to understand the molecular mechanisms of drug resistance in cervical cancer and as a tool for cancer drug discovery.Keywords: cervical cancer, drug resistant cell line, paclitaxel resistant cells, stepwise escalating concentration.


2020 ◽  
Vol 21 (7) ◽  
pp. 2619 ◽  
Author(s):  
Dominika Kazmierczak ◽  
Karol Jopek ◽  
Karolina Sterzynska ◽  
Barbara Ginter-Matuszewska ◽  
Michal Nowicki ◽  
...  

Ovarian cancer rates the highest mortality among all gynecological malignancies. The main reason for high mortality is the development of drug resistance. It can be related to increased expression of drug transporters and increased expression of extracellular matrix (ECM) proteins. Our foremost aim was to exhibit alterations in the miRNA expression levels in cisplatin (CIS), paclitaxel (PAC), doxorubicin (DOX), and topotecan (TOP)—resistant variants of the W1 sensitive ovarian cancer cell line—using miRNA microarray. The second goal was to identify miRNAs responsible for the regulation of drug-resistant genes. According to our observation, alterations in the expression of 40 miRNAs were present. We could observe that, in at least one drug-resistant cell line, the expression of 21 miRNAs was upregulated and that of 19 miRNAs was downregulated. We identified target genes for 22 miRNAs. Target analysis showed that miRNA regulates key genes responsible for drug resistance. Among others, we observed regulation of the ATP-binding cassette subfamily B member 1 gene (ABCB1) in the paclitaxel-resistant cell line by miR-363 and regulation of the collagen type III alpha 1 chain gene (COL3A1) in the topotekan-resistant cell line by miR-29a.


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