Establishment of Paclitaxel-Resistant Cell Line and the Underlying Mechanism on Drug Resistance

2012 ◽  
pp. 1 ◽  
Author(s):  
Jingjing Zhang ◽  
Jin Zhao ◽  
Wenjing Zhang ◽  
Guanyuan Liu ◽  
Dongmei Yin ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Cell Line ◽  
Underlying Mechanism ◽  
Resistant Cell ◽  
Resistant Cell Line

Understanding Cancer Drug Resistance by Developing and Studying Resistant Cell Line Models

2016 ◽  
Vol 16 (3) ◽  
pp. 226-237 ◽  
Author(s):  
Cristina P.R. Xavier ◽  
Milica Pesic ◽  
M. Helena Vasconcelos
Keyword(s):  
Drug Resistance ◽  
Cell Line ◽  
Resistant Cell ◽  
Resistant Cell Line ◽  
Cancer Drug ◽  
Cancer Drug Resistance

Lentivirus-mediated RNA interference reversing the drug-resistance in MDR1 single-factor resistant cell line K562/MDR1

2009 ◽  
Vol 33 (8) ◽  
pp. 1114-1119 ◽  
Author(s):  
Xueshi Ye ◽  
Ting Liu ◽  
Yuping Gong ◽  
Bohui Zheng ◽  
Wentong Meng ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Rna Interference ◽  
Cell Line ◽  
Resistant Cell ◽  
Resistant Cell Line ◽  
Single Factor

scholarly journals The Significance of MicroRNAs Expression in Regulation of Extracellular Matrix and Other Drug Resistant Genes in Drug Resistant Ovarian Cancer Cell Lines

2020 ◽  
Vol 21 (7) ◽  
pp. 2619 ◽  
Author(s):  
Dominika Kazmierczak ◽  
Karol Jopek ◽  
Karolina Sterzynska ◽  
Barbara Ginter-Matuszewska ◽  
Michal Nowicki ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Extracellular Matrix ◽  
Drug Resistance ◽  
Cell Line ◽  
Cancer Cell ◽  
Ovarian Cancer Cell ◽  
Resistant Cell ◽  
Resistant Cell Line ◽  
Drug Resistant ◽  
Resistant Genes

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.

scholarly journals LncRNA MIR4435-2HG mediates cisplatin resistance in HCT116 cells by regulating Nrf2 and HO-1

PLoS ONE ◽  
2020 ◽  
Vol 15 (11) ◽  
pp. e0223035
Author(s):  
Ping Luo ◽  
Shugui Wu ◽  
Kaibao Ji ◽  
Xia Yuan ◽  
Hongmi Li ◽  
...  
Keyword(s):  
Cell Line ◽  
Cisplatin Resistance ◽  
Hct116 Cell ◽  
Cancer Cell Line ◽  
Underlying Mechanism ◽  
Colon Cancer Cell Line ◽  
Resistant Cell ◽  
Resistant Cell Line ◽  
Mrna Levels ◽  
Hct116 Cells

Purpose Cisplatin resistance is still a serious problem in the clinic. However, the underlying mechanism remains unknown. In our study, we investigated cisplatin resistance by using the cisplatin-resistant cell line HCT116R. Methods The HCT116 cell line, a colon cancer cell line, was purchased. Cell viability was determined using CCK-8 Assay Kit. The gene expression levels of MIR4435-2HG, Nrf2, and HO-1, and caspase activity were determined using qRT-PCR and Caspase 3 Assay Kit, respectively. Results In this study, we found that the levels of the lncRNA MIR4435-2HG were dramatically increased in the cisplatin-resistant cell line HCT116R. Knockdown of MIR4435-2HG in HCT116R cells significantly restored the sensitivity to cisplatin, inhibited cell proliferation and promoted cell apoptosis. Furthermore, Nrf2 and HO-1 mRNA levels, as critical molecules in the oxidative stress pathway, were inhibited by siRNAs targeting MIR4435-2HG, suggesting that MIR4435-2HG-mediated cisplatin resistance occurs through the Nrf2/HO-1 pathway. Conclusion Our findings demonstrate that the lncRNA MIR4435-2HG is a main factor driving the cisplatin resistance of HCT116 cells.

scholarly journals Analysis of Candidate Idarubicin Drug Resistance Genes in MOLT-3 Cells Using Exome Nuclear DNA

Genes ◽  
2018 ◽  
Vol 9 (8) ◽  
pp. 390
Author(s):  
Tomoyoshi Komiyama ◽  
Atsushi Ogura ◽  
Takehito Kajiwara ◽  
Yoshinori Okada ◽  
Hiroyuki Kobayashi
Keyword(s):  
Drug Resistance ◽  
Amino Acid ◽  
Acute Leukemia ◽  
Cell Line ◽  
Nuclear Dna ◽  
Leukemia Cell ◽  
Resistant Cell ◽  
Resistant Cell Line ◽  
Leukemia Cell Line ◽  
Amino Acid Mutations

Various gene alterations related to acute leukemia are reported to be involved in drug resistance. We investigated idarubicin (IDR) resistance using exome nuclear DNA analyses of the human acute leukemia cell line MOLT-3 and the derived IDR-resistant cell line MOLT-3/IDR. We detected mutations in MOLT-3/IDR and MOLT-3 using both Genome Analysis Toolkit (GATK) and SnpEff program. We found 8839 genes with specific mutations in MOLT-3/IDR and 1162 genes with accompanying amino acid mutations. The 1162 genes were identified by exome analysis of polymerase-related genes using Kyoto Encyclopedia of Genes and Genomes (KEGG) and, among these, we identified genes with amino acid changes. In resistant strains, LIG and helicase plurality genes showed amino-acid-related changes. An amino acid mutation was also confirmed in polymerase-associated genes. Gene ontology (GO) enrichment testing was performed, and lipid-related genes were selected from the results. Fluorescent activated cell sorting (FACS) was used to determine whether IDR permeability was significantly different in MOLT-3/IDR and MOLT-3. The results showed that an IDR concentration of 0.5 μg/mL resulted in slow permeability in MOLT-3/IDR. This slow IDR permeability may be due to the effects of amino acid changes in polymerase- and lipid-associated genes.

scholarly journals Molecular mechanism of acquired drug resistance in the EGFR‐TKI resistant cell line HCC827‐TR

2020 ◽  
Vol 11 (5) ◽  
pp. 1129-1138
Author(s):  
Tao Yu ◽  
Qian Xia ◽  
Ting Gong ◽  
Jing Wang ◽  
DianSheng Zhong
Keyword(s):  
Drug Resistance ◽  
Cell Line ◽  
Molecular Mechanism ◽  
Resistant Cell ◽  
Resistant Cell Line ◽  
Acquired Drug Resistance ◽  
Egfr Tki
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