The difference between multi-drug resistant cell line A549/Gem and its parental cell A549

2009 ◽  
Vol 8 (4) ◽  
pp. 190-194 ◽  
Author(s):  
Weixia Wang ◽  
Xiaoqing Liu ◽  
Chuanhao Tang
Keyword(s):  
Cell Line ◽  
Parental Cell ◽  
Resistant Cell ◽  
Resistant Cell Line ◽  
Drug Resistant ◽  
The Difference ◽  
Drug Resistant Cell

The difference between multi-drug resistant cell line H460/Gem and its parental cell NCI-H460

2008 ◽  
Vol 7 (11) ◽  
pp. 615-619 ◽  
Author(s):  
Weixia Wang ◽  
Xiaoqing Liu ◽  
Guangxian Liu ◽  
Chuanhao Tang ◽  
Lili Qu ◽  
...  
Keyword(s):  
Cell Line ◽  
Parental Cell ◽  
Resistant Cell ◽  
Resistant Cell Line ◽  
Drug Resistant ◽  
The Difference ◽  
Drug Resistant Cell

An immortalized drug-resistant cell line established from 12–13-day mouse embryos for the propagation of human embryonic stem cells

2006 ◽  
Vol 74 (4) ◽  
pp. 160-166 ◽  
Author(s):  
Shiro Iuchi ◽  
Meytha Marsch-Moreno ◽  
Cristina Velez-DelValle ◽  
Karen Easley ◽  
Walid Kuri-Harcuch ◽  
...  
Keyword(s):  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Cell Line ◽  
Human Embryonic Stem Cells ◽  
Embryonic Stem ◽  
Resistant Cell ◽  
Resistant Cell Line ◽  
Mouse Embryos ◽  
Drug Resistant ◽  
Drug Resistant Cell

A serine 37 mutation associated with two missense mutations at highly conserved regions of p53 affect pro-apoptotic genes expression in a T-lymphoblastoid drug resistant cell line

Oncogene ◽  
2000 ◽  
Vol 19 (44) ◽  
pp. 5098-5105 ◽  
Author(s):  
Caterina Cinti ◽  
Pier Paolo Claudio ◽  
Antonio De Luca ◽  
Monica Cuccurese ◽  
Candace M Howard ◽  
...  
Keyword(s):  
Cell Line ◽  
Resistant Cell ◽  
Resistant Cell Line ◽  
Drug Resistant ◽  
Missense Mutations ◽  
Conserved Regions ◽  
Genes Expression ◽  
Apoptotic Genes ◽  
Drug Resistant Cell

scholarly journals Understanding the Role of Extracellular Vesicles in Lenalidomide-Resistance Multiple Myeloma

Blood ◽  
2018 ◽  
Vol 132 (Supplement 1) ◽  
pp. 1887-1887
Author(s):  
Tomofumi Yamamoto ◽  
Nobuyoshi Kosaka ◽  
Ochiya Takahiro ◽  
Yutaka Hattori
Keyword(s):  
Bone Marrow ◽  
Drug Resistance ◽  
Cell Line ◽  
Cell Lines ◽  
Parental Cell ◽  
Resistant Cell ◽  
Bone Marrow Microenvironment ◽  
Drug Resistant ◽  
Apoptosis Assay ◽  
Drug Resistant Cell

Abstract Multiple myeloma (MM) is a plasma cell malignancy that develops by the accumulation of various genetic abnormalities. In recent years, the prognosis of MM has improved by the development of novel drugs including immunomodulatory drugs (IMiDs), proteasome inhibitors, and antibody drugs. However, MM cells acquired drug resistance by long-term exposure to these therapeutic drugs. MM is a multiclonal disease, and various clone subtypes develop within the bone marrow microenvironment. It has been suggested that drug resistant phenotype could transmit from resistant clones to sensitive ones, and also to immune cells, or mesenchymal stem cells, resulting in the change of bone marrow microenvironment suitable for MM cell survival. It has been shown that extracellular vesicles (EVs) are one of the means of information transmission. EVs are secreted from almost all cells, and the amount of EV secretion is particular high from cancer cells. It was already known that cancer-derived EVs transmitted information associated with cancer progressions such as angiogenesis, metastasis, and drug resistance to the surrounding cells. Thus, EVs were proposed to play an important role in acquisition of drug resistance even though the mechanisms have not been fully understood in MM. In order to understand the mechanism of drug resistance in MM mediated by EVs, lenalidomide resistant cell lines were established by long-term exposure of lenalidomide. The amount of EVs was measured by ExoScreen, which is ultra-sensitive detection method of EVs by measuring surface protein of EVs, such as, CD9 and CD63, and by the nanoparticle tracking analysis. We found that lenalidomide resistant cell lines in KMS21R, KMS27R and KMS34R cell lines secreted about twice more EVs than their parental cell lines, and the amount of EV secretion was correlated with the drug sensitivity of lenalidomide. Suppression of EV secretion by knockdown of TSG101, which is known for EV secretion-associated protein, did not affect lenalidomide resistance. We could suppress the EV secretion to two-thirds, however cell proliferation and caspase activity were not change. From these results, we postulated the two possibilities; 1) EV secretion pathway other than TSG101 is associated with drug resistance via EVs; 2) EV derived from lenalidomide resistant cells can affect the cells exist in bone marrow microenvironment. From these hypotheses, we have done the following experiments. Firstly, to identify the genes which involved in EV secretion pathway associated with drug resistance, RNA sequence among the drug-resistant cell lines and their parental cell lines was performed. Drug resistant cell lines had some genetic abnormality, for instance immune system or angiogenesis. Now, we are detecting the EV secretion associated genes in drug resistant cell lines. Secondly, EV derived from the drug-resistant cell lines and EV derived from the parent cell lines were added to drug sensitive MM cell lines, then lenalidomide is added after 24hr. The cell proliferation and apoptosis assay were evaluated after 48hr. EV derived from the drug-resistant cell lines in KMS34R cell line significantly inhibited cell death measured by MTS assay and apoptosis assay compared with those from the drug sensitive KMS21 and KMS34 cell lines. EVs from KMS34R cell line, which is the most progressed cell line we established, could more transmit drug resistance than those from other cell lines. These results suggested that drug resistance was transmitted from drug-resistant cell lines to non-resistant cell lines via EVs. Now, we are analyzing the component of EV from drug-resistant MM cells by proteome analysis to identify the molecules associated with lenalidomide resistance in MM. In addition, we are investigating the molecules which associated with the secretion of EVs from drug-resistance MM. These results prompted us to hypothesize that attenuating the function of a molecule responsible for EV secretion could lead to the inhibition of cancer development such as drug resistance. It is expected that EVs will be novel therapeutic targets in refractory or relapsed MM. Disclosures Hattori: IDAC inc.: Research Funding; Takeda: Research Funding.

Characterization of promoter elements involved in the down-regulation of topoisomerase IIα expression in a drug-resistant cell line

Gene ◽  
2004 ◽  
Vol 342 (1) ◽  
pp. 145-155 ◽  
Author(s):  
Deepa Saxena ◽  
Gary K. Yiu ◽  
Xiaoyan Ni ◽  
Kuan-Chun Huang ◽  
Roberto Mantovani ◽  
...  
Keyword(s):  
Cell Line ◽  
Resistant Cell ◽  
Resistant Cell Line ◽  
Drug Resistant ◽  
Promoter Elements ◽  
Down Regulation ◽  
Topoisomerase Iiα ◽  
Drug Resistant Cell
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