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KMID : 0620920160480120002
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Experimental & Molecular Medicine
2016 Volume.48 No. 12 p.2 ~ p.2
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Migration and invasion of drug-resistant lung adenocarcinoma cells are dependent on mitochondrial activity
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Jeon Ji-Hoon
Kim Dong-Keon
Shin Young-mi
Kim Hee-Yeon
Song Bo-min
Lee Eun-Young
Kim Jong-Kwang
You Hye-Jin
Cheong Hee-sun
Shin Dong-Hoon
Kim Seong-Tae
Cheong Jae-Ho
Kim Soo-Youl
Jang Hyon-Chol
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Abstract
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A small proportion of cancer cells have stem-cell-like properties, are resistant to standard therapy and are associated with a poor prognosis. The metabolism of such drug-resistant cells differs from that of nearby non-resistant cells. In this study, the metabolism of drug-resistant lung adenocarcinoma cells was investigated. The expression of genes associated with oxidative phosphorylation in the mitochondrial membrane was negatively correlated with the prognosis of lung adenocarcinoma. Because the mitochondrial membrane potential (MMP) reflects the functional status of mitochondria and metastasis is the principal cause of death due to cancer, the relationship between MMP and metastasis was evaluated. Cells with a higher MMP exhibited greater migration and invasion than those with a lower MMP. Cells that survived treatment with cisplatin, a standard chemotherapeutic drug for lung adenocarcinoma, exhibited increased MMP and enhanced migration and invasion compared with parental cells. Consistent with these findings, inhibition of mitochondrial activity significantly impeded the migration and invasion of cisplatin-resistant cells. RNA-sequencing analysis indicated that the expression of mitochondrial complex genes was upregulated in cisplatin-resistant cells. These results suggested that drug-resistant cells have a greater MMP and that inhibition of mitochondrial activity could be used to prevent metastasis of drug-resistant lung adenocarcinoma cells.
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KEYWORD
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