Down-regulation of the JAK2/PI3K-mediated signaling activation is involved in Taiwan cobra cardiotoxin III-induced apoptosis of human breast MDA-MB-231 cancer cells

Lin, Kuei Li; Su, Jun-Ming; Chien, Ching Ming; Chuang, Pei Wen; Chang, Long; Lin, Shinne Ren

doi:10.1016/j.toxicon.2010.01.017

Cited by 48 publications

(22 citation statements)

References 40 publications

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“…For other types of cancer cells, the antiproliferation and apoptosis-inducible effects of CTXIII have been reported [12–16, 23, 24]. The detailed mechanism of CTXIII-induced apoptosis have well demonstrated, such as mitochondrial alteration, reactive oxygen species generation of neuroblastoma SK-N-SH cells [23], NF- κ B inactivation in breast MCF-7 cancer cells [12], and downregulation of the JAK2/PI3K signaling in breast MDA-MB-231 cancer cells [24].…”

Section: Discussionmentioning

confidence: 99%

Cardiotoxin III Inhibits Proliferation and Migration of Oral Cancer Cells through MAPK and MMP Signaling

Yen

Liang

Han

et al. 2013

The Scientific World Journal

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Cardiotoxin III (CTXIII), isolated from the snake venom of Formosan cobra Naja naja atra, has previously been found to induce apoptosis in many types of cancer. Early metastasis is typical for the progression of oral cancer. To modulate the cell migration behavior of oral cancer is one of the oral cancer therapies. In this study, the possible modulating effect of CTXIII on oral cancer migration is addressed. In the example of oral squamous carcinoma Ca9-22 cells, the cell viability was decreased by CTXIII treatment in a dose-responsive manner. In wound-healing assay, the cell migration of Ca9-22 cells was attenuated by CTXIII in a dose- and time-responsive manner. After CTXIII treatment, the MMP-2 and MMP-9 protein expressions were downregulated, and the phosphorylation of JNK and p38-MAPK was increased independent of ERK phosphorylation. In conclusion, CTXIII has antiproliferative and -migrating effects on oral cancer cells involving the p38-MAPK and MMP-2/-9 pathways.

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Section: Discussionmentioning

confidence: 99%

Cardiotoxin III Inhibits Proliferation and Migration of Oral Cancer Cells through MAPK and MMP Signaling

Yen

Liang

Han

et al. 2013

The Scientific World Journal

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“…Cells were harvested, washed, and resuspended as described previously (Lin et al, 2010a(Lin et al, , 2010b. Controlled and treated cells were harvested, washed in cold phosphate-buffered saline (PBS), fixed in 70% ethanol, and stored at 4°C.…”

Section: Cell Cycle Analysismentioning

confidence: 99%

“…In our previous study, CTX III has shown antitumor activity, inhibiting the growth of several types of cultured human cancer cells. In recent years, putative mechanisms of growth inhibition included cell cycle arrest Yang et al, 2007), involvement of both endoplasmic reticulum-and mitochondriadependent pathways (Chien et al, 2008), inactivation of c-Jun Nterminal kinase (Yang et al, 2007) and NF-κB (Chiu et al, 2009), and down-regulation of the JAK2/PI3K-mediated signaling activation (Lin et al, 2010a(Lin et al, , 2010b. However, the capacity of CTX III to inhibit the metastasis of malignant carcinoma is still unknown.…”

Section: Introductionmentioning

confidence: 99%

Antimetastatic potential of cardiotoxin III involves inactivation of PI3K/Akt and p38 MAPK signaling pathways in human breast cancer MDA-MB-231 cells

et al. 2012

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“…However, the effectiveness of chemotherapy is reduced due to the toxic side effects. Studies in vivo and in vitro have shown that membrane toxin (MT) is capable of killing a variety of tumor cells (2,3). Its anti-tumor mechanism is not yet completely understood, yet recent studies have shown that the destruction of the cell membrane structure and interference with DNA synthesis may be involved.…”

Section: Introductionmentioning

confidence: 99%

“…Research also suggest that MT may be able to induce tumor cell apoptosis (4). Research of the effects of MT on liver, lung, breast, melanoma and colorectal cancer is common (2,3,5). However, there are few studies that have been carried out on bladder cancer.…”

Section: Introductionmentioning

confidence: 99%

Effect of membrane toxin 12 isolated from Naja naja atra on proliferation and invasion of human bladder cancer EJ cells

Yang

Wang

et al. 2011

Mol Med Report

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Abstract.We investigated the effect of membrane toxin 12 (MT-12), isolated from Naja naja atra, a species of Chinese Cobra, on the proliferation and invasion of human bladder cancer EJ cells and studied its mechanisms using MTT assay, Transwell chamber invasion assay, scanning electron microscopy and flow cytometry. The results indicated that MT-12 inhibited the proliferation of bladder cancer cells in a dose-dependent manner. The half maximal inhibitory concentration (IC 50 ) after 72 h was 0.66 µg/ml. The invasion of cells decreased with increasing doses of MT-12 (0.125-0.5 µg/ml, P<0.001). Expression of CXCR4 decreased with the effect of MT-12 for a particular concentration range (0.125-0.5 µg/ml). To conclude, MT-12 is capable of inhibiting the proliferation and invasion of bladder cancer EJ cells. This mechanism may be associated with reduced expression of CXCR4 protein. IntroductionInvasion and metastasis are distinct features of malignant tumors, and metastasis is the main reason for failure of cancer treatment. Invasion and metastasis are affected by numerous factors, including the induction of angiogenesis, stroma adhesion, protein hydrolysis and movement, among others (1). Urinary bladder cancer is one of the most common types of cancer, and postoperative chemotherapy remains the most important auxiliary treatment method. However, the effectiveness of chemotherapy is reduced due to the toxic side effects. Studies in vivo and in vitro have shown that membrane toxin (MT) is capable of killing a variety of tumor cells (2,3). Its anti-tumor mechanism is not yet completely understood, yet recent studies have shown that the destruction of the cell membrane structure and interference with DNA synthesis may be involved. Research also suggest that MT may be able to induce tumor cell apoptosis (4). Research of the effects of MT on liver, lung, breast, melanoma and colorectal cancer is common (2,3,5). However, there are few studies that have been carried out on bladder cancer. This experimental study of the effects of purified membrane toxin 12 (MT-12) on the human bladder cancer EJ cell line is reported as follows. Study apparatus and reagents were obtained as follows: FACSCalibur flow cytometer (Becton Dickinson Co., USA); a 5% CO 2 incubator and centrifuge volume fraction (ThermoFisher Scientific, Germany); a Bio-Rad 450 microplate reader, an electronic balance (Test Instrument Changshu Double Jay); and an S-3000N scanning electron microscope; a volume fraction of 2.5% glutaraldehyde; mouse anti-human CXCR4 fluorescent antibody (Santa Cruz Biotechnology, Inc., CA, USA); CXCR4 goat anti-mouse monoclonal antibody (Santa Cruz Biotechnology, Inc.); RPMI-1640 (Gibco, Invitrogen, Paisley, UK). Materials and methods MaterialsCell culture. The improved MTT method was used to study the effect of MT-12 on the proliferation of EJ cells as previously described (6). After the EJ cells reached the logarithmic growth phase, the cell concentration was adjusted to 5x10 4 /ml and the cells were added into a 96-well plate, 90 µl...

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Down-regulation of the JAK2/PI3K-mediated signaling activation is involved in Taiwan cobra cardiotoxin III-induced apoptosis of human breast MDA-MB-231 cancer cells

Cited by 48 publications

References 40 publications

Cardiotoxin III Inhibits Proliferation and Migration of Oral Cancer Cells through MAPK and MMP Signaling

Cardiotoxin III Inhibits Proliferation and Migration of Oral Cancer Cells through MAPK and MMP Signaling

Antimetastatic potential of cardiotoxin III involves inactivation of PI3K/Akt and p38 MAPK signaling pathways in human breast cancer MDA-MB-231 cells

Effect of membrane toxin 12 isolated from Naja naja atra on proliferation and invasion of human bladder cancer EJ cells

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