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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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Chromosomal instability in PC-6 small-cell lung cancer cells and 7-ethyl-10-hydroxycamptothesin-resistant (PC-6/SN-38) cells. Chromosomal instability was detected in PC-6/SN-38 and compared to that in PC-6. Dual-color FISH (CEP7 [green]/c-MET [red]) was carried out on fixed cell specimens from PC-6 (a) and PC-6/SN-38 (b) cells. The number of CEP7 and c-MET signals in 100 cells was listed (c). 20× maginification.
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fig05: Chromosomal instability in PC-6 small-cell lung cancer cells and 7-ethyl-10-hydroxycamptothesin-resistant (PC-6/SN-38) cells. Chromosomal instability was detected in PC-6/SN-38 and compared to that in PC-6. Dual-color FISH (CEP7 [green]/c-MET [red]) was carried out on fixed cell specimens from PC-6 (a) and PC-6/SN-38 (b) cells. The number of CEP7 and c-MET signals in 100 cells was listed (c). 20× maginification.

Mentions: We examined c-MET gene amplification or chromosomal instability in PC-6 and PC-6/SN-38 cells by FISH analysis. Diploid cells accounted for 95% (95 cells/100 cells) and tetraploid only 1% (1 cell/100 cells) of all PC-6 cells (Fig. 5a,c), whereas diploid cells accounted for 35% (35 cells/100 cells), triploid 7% (7 cells/100 cells), and tetraploid 48% (48 cells/100 cells) of all PC-6/SN-38 cells (Fig. 5b,c). In addition, the copy number of the c-MET gene increased by one as compared with CEP7 in 6% of PC-6/SN-38 cells relative to PC-6 cells (Fig. 5c).


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)

Chromosomal instability in PC-6 small-cell lung cancer cells and 7-ethyl-10-hydroxycamptothesin-resistant (PC-6/SN-38) cells. Chromosomal instability was detected in PC-6/SN-38 and compared to that in PC-6. Dual-color FISH (CEP7 [green]/c-MET [red]) was carried out on fixed cell specimens from PC-6 (a) and PC-6/SN-38 (b) cells. The number of CEP7 and c-MET signals in 100 cells was listed (c). 20× maginification.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4317853&req=5

fig05: Chromosomal instability in PC-6 small-cell lung cancer cells and 7-ethyl-10-hydroxycamptothesin-resistant (PC-6/SN-38) cells. Chromosomal instability was detected in PC-6/SN-38 and compared to that in PC-6. Dual-color FISH (CEP7 [green]/c-MET [red]) was carried out on fixed cell specimens from PC-6 (a) and PC-6/SN-38 (b) cells. The number of CEP7 and c-MET signals in 100 cells was listed (c). 20× maginification.
Mentions: We examined c-MET gene amplification or chromosomal instability in PC-6 and PC-6/SN-38 cells by FISH analysis. Diploid cells accounted for 95% (95 cells/100 cells) and tetraploid only 1% (1 cell/100 cells) of all PC-6 cells (Fig. 5a,c), whereas diploid cells accounted for 35% (35 cells/100 cells), triploid 7% (7 cells/100 cells), and tetraploid 48% (48 cells/100 cells) of all PC-6/SN-38 cells (Fig. 5b,c). In addition, the copy number of the c-MET gene increased by one as compared with CEP7 in 6% of PC-6/SN-38 cells relative to PC-6 cells (Fig. 5c).

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