JB6 cell line

A second bioassay, a soft agar transformation assay, has been utilized at the University of Illinois at Chicago to determine the inhibition of transformation of the JB6 cell line by treatment of the test materials [88]. The primary epidermal cell cultures from newborn BALB/c mice have been previously well developed for use as a tool in chemical... 

Studies with JB6 mouse epidermal cells demonstrated that resveratrol agly-cone-induced apoptosis in these cells was through p53 and that it was not dependent upon normal sphingomyelinase activity as the induction of apoptosis was observed in sphingomyelinase deficient and sufficient cell lines. Studies by Lu,... 

In the JB6 mouse epidermal cell line, the tumor promoter TPA causes cell transformation at high frequency, marked induced NFkB activation. EGCG and TF-3 inhibited TPA-induced NFkB activity in a concentration-dependent manner. These tea polyphenols blocked TPA-induced phosphorylation of IkB at Ser 32 in the same concentration range. Moreover, the NFkB sequence-specific DNA binding activity induced by TPA was also inhibited by these polyphenols. These results confirmed that inhibition of NFkB activation is also important in evaluation of the antitumor promotion effects of tea polyphenols. 

Muehlematter D, Ochi T, Cerutti P (1989) Effects of tert-butyl hydroperoxide on promotable and non-promotable JB6 mouse epidermal cells. Chem Biol Interact 71 339-352 Nose K, Shibanuma M, Kikuchi K, Kageyama H, Sakiyama S, Kuroki T (1991) Transcriptional activation of early-response genes by hydrogen peroxide in a mouse osteoblastic cell line. Eur J Biochem 201 99-106... 

Low levels (0.1-1 pg/mL) of resveratrol have been reported to enhance cell proliferation, whereas higher amounts (10-100 pg/mL) cause apoptosis in a vari-ety of tumor and endothelial cells, including JB6 epidermal cells, human promyeloctye leukemia HL-60 cells, THP-1 human monocytic leukemia cells, U937 human promonocytic cells, various colon cancer cell lines, human mammary cancer cell lines, and human prostate cancer cells [121-131]. In somewhat of a contrast to these studies, a very recent report indicated that resveratrol reduced paclitaxel-induced apoptosis in a human neuroblastoma cell line (SH-SY5Y) by blocking paclitaxel-induced phosphorylation of JNKs, Raf-1, and BcT2 [132]. Of particular interest is a recent study in which it was shown to induce apoptosis in leukemic human lymphocytes but, under similar conditions, had no effect on the survival... 

On the basis of the studies reported above, a possible mechanism may involve extracellular signal-regulated protein kinases (ERKs) and p38 kinase-mediated p53 activation and induction of apoptosis [148, 160] (Fig. 2). In the mouse JB6 epidermal cell line [161, 162], resveratrol induced apoptosis to inhibit tumor promoter-induced cell transformation through enhanced transactivation of p53 activity [148]. Resveratrol-induced activation of p53 and apoptosis was shown to be dependent on the activities of... 

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. ... 

Dong et al. (1997) used JB6 mouse epidermal cell line, a system that has extensively been used as an in vitro model for tumor promotion studies, to examine antitumor promotion effects of EGCG and theaflavins at the molecular levels. EGCG and theaflavins inhibited EGF- or TP A- induced cell transformation in a dose-dependent manner. EGCG and theaflavins also inhibited AP-1-dependent transcriptional activity and DNA binding activity. This study further showed that the inhibition of AP-1 activation occurs through the inhibition of a c-Jun NH2-terminal kinase dependent pathway. 

Anthocyanins JB6 P mouse epidermal cell line Blocks activation of the MAPK pathway. [86]... 

JB6 C141 cells mouse epidermal cell line... 

Crocidolite JB6 mouse epithelial cell line, TRE-luciferase reporter transgenic mice Activator protein-1 activity, protein kinase phosphorylation Activator protein-1 transactivation Ding et al. (1999) ... 

Caffeic acid phenethyl ester (CAPE), an active component extracted from honeybee propolis, blocks tumorigenesis in a two-stage model of mouse skin cancer that was promoted by treatment with TP A (49). The anti-cancer or antitumor promotion effects of CAPE may be based on their ability to induce apoptosis. We foimd that CAPE suppresses TPA-induced cell transformation and induced apoptosis in mouse epidermal JB6 Cl 41 cells (50). No difference in induction of apoptosis was observed between normal lymphoblasts and sphingomyelinase-deficient cell lines. Although CAPE treatment of two p53 mutant tumor cell lines, NCI-H358 and SK-OV-3, and p53 cells caused... 

EGCG abrogated TPA-induced activation of protein kinase C, c-jun expression and transformation in cultured mouse fibroblasts in culture (22). EGCG and theaflavins inhibited EGF- or TPA- induced transformation of JB6 mouse epidermal cell line which was associated with their expression of AP-1-dependent transcriptional activity and its DNA binding activity (25). The inhibition of AP-1 activation by these substances appears to be mediated via down-regulation of INK, but not the ERK pathway. 

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