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Significance of c-MET overexpression in cytotoxic anticancer drug-resistant small-cell lung cancer cells.

Ozasa H, Oguri T, Maeno K, Takakuwa O, Kunii E, Yagi Y, Uemura T, Kasai D, Miyazaki M, Niimi A - Cancer Sci. (2014)

Bottom Line: The c-MET receptor tyrosine kinase is the receptor for hepatocyte growth factor.Furthermore, the number of c-MET gene loci was increased in the resistant cells compared to the parental cells.Our results add a new strategy, the targeting of c-MET, for overcoming resistance to cytotoxic agents in small-cell lung cancer.

View Article: PubMed Central - PubMed

Affiliation: Department of Medical Oncology and Immunology, Nagoya City University, Nagoya, Japan; Department of Multidisciplinary Cancer Treatment, Kyoto University Graduate School of Medicine, Kyoto, Japan.

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Increased c-MET DNA copy numbers in PC-6 human small-cell lung cancer cells resistant to 7-ethyl-10-hydroxycamptothesin (PC-6/SN-38), paclitaxel (PC-6/TXL), and cisplatin (PC-6/CDDP), as well as the NCI-H69 and TXL-resistant NCI-H69 (H69/TXL) small-cell lung cancer cell lines. (a) c-MET DNA copy numbers in drug-resistant cells were examined relative to the parental cells by quantitative real-time PCR. (b) c-MET DNA copy numbers in PC-6 cells, exposed to 7-ethyl-10-hydroxycamptothesin (SN-38, 5 nM) or paclitaxel (TXL, 10 nM) for 7 days, were examined by quantitative real-time PCR. *P < 0.05.
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fig04: Increased c-MET DNA copy numbers in PC-6 human small-cell lung cancer cells resistant to 7-ethyl-10-hydroxycamptothesin (PC-6/SN-38), paclitaxel (PC-6/TXL), and cisplatin (PC-6/CDDP), as well as the NCI-H69 and TXL-resistant NCI-H69 (H69/TXL) small-cell lung cancer cell lines. (a) c-MET DNA copy numbers in drug-resistant cells were examined relative to the parental cells by quantitative real-time PCR. (b) c-MET DNA copy numbers in PC-6 cells, exposed to 7-ethyl-10-hydroxycamptothesin (SN-38, 5 nM) or paclitaxel (TXL, 10 nM) for 7 days, were examined by quantitative real-time PCR. *P < 0.05.

Mentions: We examined the c-MET DNA copy number in the cytotoxic anticancer drug-resistant cells compared with the parental cells by PCR. The relative c-MET DNA copy numbers of the resistant cells was significantly increased compared with the parental cells (Fig. 4a). In addition, we examined the c-MET gene amplification in the PC-6 cells at 7 days after exposure to SN-38 (5 nM) or TXL (10 nM). The c-MET gene amplification in the PC-6 cells exposed to SN-38 or TXL was significantly increased relative to the cells not exposed (Fig. 4b).


Significance of c-MET overexpression in cytotoxic anticancer drug-resistant small-cell lung cancer cells.

Ozasa H, Oguri T, Maeno K, Takakuwa O, Kunii E, Yagi Y, Uemura T, Kasai D, Miyazaki M, Niimi A - Cancer Sci. (2014)

Increased c-MET DNA copy numbers in PC-6 human small-cell lung cancer cells resistant to 7-ethyl-10-hydroxycamptothesin (PC-6/SN-38), paclitaxel (PC-6/TXL), and cisplatin (PC-6/CDDP), as well as the NCI-H69 and TXL-resistant NCI-H69 (H69/TXL) small-cell lung cancer cell lines. (a) c-MET DNA copy numbers in drug-resistant cells were examined relative to the parental cells by quantitative real-time PCR. (b) c-MET DNA copy numbers in PC-6 cells, exposed to 7-ethyl-10-hydroxycamptothesin (SN-38, 5 nM) or paclitaxel (TXL, 10 nM) for 7 days, were examined by quantitative real-time PCR. *P < 0.05.
© Copyright Policy - open-access
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4317853&req=5

fig04: Increased c-MET DNA copy numbers in PC-6 human small-cell lung cancer cells resistant to 7-ethyl-10-hydroxycamptothesin (PC-6/SN-38), paclitaxel (PC-6/TXL), and cisplatin (PC-6/CDDP), as well as the NCI-H69 and TXL-resistant NCI-H69 (H69/TXL) small-cell lung cancer cell lines. (a) c-MET DNA copy numbers in drug-resistant cells were examined relative to the parental cells by quantitative real-time PCR. (b) c-MET DNA copy numbers in PC-6 cells, exposed to 7-ethyl-10-hydroxycamptothesin (SN-38, 5 nM) or paclitaxel (TXL, 10 nM) for 7 days, were examined by quantitative real-time PCR. *P < 0.05.
Mentions: We examined the c-MET DNA copy number in the cytotoxic anticancer drug-resistant cells compared with the parental cells by PCR. The relative c-MET DNA copy numbers of the resistant cells was significantly increased compared with the parental cells (Fig. 4a). In addition, we examined the c-MET gene amplification in the PC-6 cells at 7 days after exposure to SN-38 (5 nM) or TXL (10 nM). The c-MET gene amplification in the PC-6 cells exposed to SN-38 or TXL was significantly increased relative to the cells not exposed (Fig. 4b).

Bottom Line: The c-MET receptor tyrosine kinase is the receptor for hepatocyte growth factor.Furthermore, the number of c-MET gene loci was increased in the resistant cells compared to the parental cells.Our results add a new strategy, the targeting of c-MET, for overcoming resistance to cytotoxic agents in small-cell lung cancer.

View Article: PubMed Central - PubMed

Affiliation: Department of Medical Oncology and Immunology, Nagoya City University, Nagoya, Japan; Department of Multidisciplinary Cancer Treatment, Kyoto University Graduate School of Medicine, Kyoto, Japan.

Show MeSH
Related in: MedlinePlus