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Title: Applicability of Jurkat cell line for cancer study Post by: songtree on May 10, 2011 I want to do a comparative study between the CD4+ Jurkat T cell line and primary CD4+ T cells to study cancer. I cannot seem to find any papers using this in vitro model for cancer. Is there a reason why?
Title: Re: Applicability of Jurkat cell line for cancer study Post by: ppk on May 10, 2011 In my microbiology class, we looked into the difference between the two. To my understanding, Jurkat cells are a proliferating line of T lymphocyte cells that are used to study acute T cell leukemia, T cell signaling, and the expression of various chemokine receptors susceptible to viral entry, particularly HIV. And, unlike other cells lines, they have the ability to produce Il-2. I think the main reason why they don't typically use them in cancer studies is because they are hard to maintain. Depending on what you're studying, sometimes these cell lines can be hard to keep alive for a prolonged period of time (>month), and this makes isolating stuff like RNA a pain. Jurkat cells are also hard to transfect, and can grow very fast; in fact, if the cell density is too high, they’ll start to die off. This could be a problem when looking at things like cancer. But don't get me wrong, they are easy cells to grow as they don't require any special culturing conditions - to my knowledge. However, aside from all this, I have read that they are used extensively in the study of T-cell signaling and cancer drug development.
Check out this paper: Natural Killer (NK) Cell–mediated Cytotoxicity: Differential Use of TRAIL and Fas Ligand by Immature and Mature Primary Human NK Cells (http://jem.rupress.org/content/188/12/2375.full.pdf) This article states: Because Jurkat cells are similar to peripheral blood T cells in their activation-dependent integrin regulation through PMA, CD2, CD3, and CD28 stimulation, we used this T- cell line to ascertain whether the various integrin regulatory molecules are interdependent, or whether activation through one receptor is independent of the presence of other integrin regulatory molecules. Thus, we produced a series of... Differential Activation-Dependent Regulation of Integrin Function in Cultured Human T-Leukemic Cell Lines (http://bloodjournal.hematologylibrary.org/content/83/4/1039.full.pdf) This article states: Thus, it is possible that anti-apoptotic effects observed in Jurkat cells may not appear in activated T lymphocytes treated with IL-2, because Jurkat cells are well-known to be sensitive to various apoptotic signals. Taken together, our results suggest that galectin-3 is involved in proliferation of activated T lymphocytes mainly, although it is still possible that galectin-3 has anti-apoptotic effects. Expression and function of galectin-3, a ß-galactoside-binding protein in activated T lymphocytes (http://www.jleukbio.org/content/69/4/555.full) Characterization of EBV-genome negative “null” and “T” cell lines derived from children with acute lymphoblastic leukemia and leukemic transformed non-Hodgkin lymphoma (http://onlinelibrary.wiley.com/doi/10.1002/ijc.2910190505/abstract;jsessionid=E5D6E84B1564E371E67791A201E790B4.d02t04?systemMessage=Wiley+Online+Library+will+be+disrupted+14+May+from+10-12+BST+for+monthly+maintenance) Methotrexate Suppresses NF-kB Activation Through Inhibition of IkBalpha Phosphorylation and Degradation (http://www.jimmunol.org/content/167/5/2911.full.pdf) Jurkat T cells and development of the T-cell receptor signalling paradigm (http://www.nature.com/nri/journal/v4/n4/full/nri1330.html) CD3 receptor modulation in Jurkat leukemic cell line (http://fhc.amb.edu.pl/archives/fulltxt/vol42/42_1/Jozwik.pdf) Catharanthus roseus aqueous extract is cytotoxic to Jurkat leukaemic T-cells but induces the proliferation of normal peripheral blood mononuclear cells (http://www.tlsr.usm.my/earlyviewDetail_files/ARTICLES/TLSR-21-2-9-Hazwani.pdf) FasL is more frequently expressed in liver metastases of colorectal cancer than in matched primary carcinoma (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2362258/pdf/79-6690202a.pdf) 5-Fluorouracil-induced Death of Jurkat T-Cells – A Role for Caspases and MCL-1 (http://ar.iiarjournals.org/content/30/10/3879.full) Cell lines: --> The JCaM1.6 cell line is deficient in Lck kinase activity due to the deletion of part of the lck gene (exon 7) from the Lck transcript. --> J.RT3-T3.5 cells have a mutation in the T cell receptor beta chain locus precluding expression of this chain. This affects the cells in several ways. They do not express surface CD3 or produce the T cell receptor alpha/beta heterodimer. Since they are deficient in the TCR complex, these cells are a useful tool for transfection studies using T cell receptor alpha and beta chain genes and are widely used in labs in which T cell receptor gene transfer technologies are studied. --> The I 9.2 and I 2.1 cell lines. The I 2.1 cell line is functionally defective for FADD and the I 9.2 cell line is functionally defective for caspase-8, both defective molecules being essential to apoptosis or programmed cell death of cells. --> The D1.1 cell line does not express CD4 molecule, an important co-receptor in the activation pathway of helper T cells. --> The J.gamma1 subline contains no detectable phospholipase C-gamma1 (PLC-?1) protein and therefore has profound defects in T cell receptor (TCR) calcium mobilization, and nuclear factor of activated T-cells (NFAT) activation (an important transcription factor in T cells). I can probably download a lot of these papers for you, for free, if you cannot. Hope these resources help. |