Jurkat cells proliferation

Previous studies have reported that ERKs are characteristically associated with cell proliferation and protection from apoptosis (Bl, XI), while activation of JNK and p38 MAPK can promote apoptosis in many systems, including B lymphocytes (G5), cerebellar granule cells (K3), hematopoietic cells (K8), and neuronal cells (M3, XI). On the other hand, a recent report found that a pyridinyl imidazole, SB 202190, the specific inhibitor of p38 MAPK, by itself was sufficient to induce apoptosis in T lymphocyte Jurkat cells (N2). Moreover, Th-2-derived cytokine IL-5, the ERK activator and antiapoptotic factor for eosinophils, could also activate p38 MAPK in human eosinophils (BIO). We recently reported that cytokine IL-3, IL-5, and GM-CSF could prolong survival of human eosinophilic leukemic (EoL-1) cells through the transient activation of ERK (W15). On the other hand, activation of p38 MAPK in EoL-1 cells by the NSAID sodium salicylate (NaSal) could lead to apoptosis (W15). We also found that the suppression of ERK using ERK antisense phosphorothioate oligodeoxynucleotides could promote the apoptosis of peripheral blood eosinophils (W16). Moreover, we found that dexamethasone-induced apoptosis and activation of JNK and p38 MAPK activity in eosinophils are regulated by caspases (Z2). 

O Rourke, F. A., LaPlante, J. M. and Feinstein, M. B., 2003, Antisense-mediated loss of calcium homoeostasis endoplasmic reticulum protein (CHERP ERPROT213-21) impairs Ca2+ mobilization, nuclear factor of activated T-cells (NFAT) activation and cell proliferation in Jurkat T-lymphocytes. Biochem J 373, 133-43. 

Data on bioactivity on immunocompetent cells provide evidence that D-Ala-deltorphin-I potently (10-9 to 10-11 M) and persistently (up to 4 days) enhances Con A-induced mouse spleen cell proliferation [85]. The peptide increases uptake of thymidine and production of interferon--/ in phytohe-magglutinin-activated human lymphocytes [86] and is 100 times more potent than SNC80 in inhibiting the production of p24 antigen, an index of HIV-1 expression, in Jurkat cells stably transfected with a cDNA encoding for the delta-opiate receptor [87]. 

Studies on some cell lines have shown that in tumor models such as mouse epidermal 1B6 cells and MCF-7, ROS were observed to stimulate cell growth in monolayers. In other cell lines, ROS can also be involved in the pathogenesis of cancer. By promoting cell proliferation in the transformed cancer cell lines MCF-7, HeLa, and Jurkat cells, reduced antioxidant levels were implicated in malignant transformation. Overexpression of manganese superoxide dismutase (MnSOD), a normal cellular antioxidant, enzyme was reported to revert transformation or tumor-promotion response in these and other transformed cell tines, such as human melanoma (UACC-903) cells, human breast cancer (MCF-7) cells, and mouse epidermal JB6 cells. ... 

For example, Jurkat T cells apoptose in response to serum withdrawal, addition of exogenous cell-permeable ceramide or stimulation with the apoptotic agonist Fas. However, transfection with SPHKl, measured as a 400-600-fold increase in activity, reduced apoptosis and inaeased proliferation (Ohvera et al, 1999). These effects were correlated with an inhibition of the activity of caspase 3, an initiator caspase (Olivera et al, 1999), A similar effect has recently been observed in rat pheochromocytoma PC12 cells (Edsall etal, 2(X)1). Tropbic withdrawal led to the activation of... 

Parallel to our group, a few other researchers also performed significant studies on anticancer (3-lactams. For example, (3-lactam derivatives (Fig. 2) induced DNA damage, inhibited DNA replication, and activated the apoptotic death program in human leukemic Jurkat T cells in a time and concentration-dependent manner. Importantly, (3-lactam 69 also inhibited proliferation and induced apoptosis in other human solid tumor cell lines (breast, prostate, and head-and-neck). It was believed that induction of apoptosis by 69 is associated with activation of p38 mitogen-activated protein (MAP) kinase, release of mitochondrial cytochrome c, and activation of the caspases. It was reported that apoptosis is blocked by a specific inhibitor to p38 kinase, implicating p38 MAP kinase as the major factor in (3-lactam-induced apoptosis [154]. This study was very significant. 

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