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Impaired Growth of Telomerase-Deficient Cells by Telomere Dysfunction
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ÁÖ¿¬Áø ( Ju Yeun-Jin )
¿øÀÚ·ÂÀÇÇпø ¹æ»ç¼±ÀÇÇבּ¸¼¾ÅÍ
¹ÚÁ¤Àº ( Park Jeong-Eun )
¿øÀÚ·ÂÀÇÇпø ¹æ»ç¼±ÀÇÇבּ¸¼¾ÅÍ
Àü°æ¹Ì ( Juhn Kyoung-Mi )
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±èâ¹Î ( Kim Chang-Min )
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±è»óÈÆ ( Kim Sang-Hoon )
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¹Ú¿øºÀ ( Park Won-Bong )
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À̱âÈ£ ( Lee Kee-Ho )
¿øÀÚ·ÂÀÇÇпø ¹æ»ç¼±ÀÇÇבּ¸¼¾ÅÍ
KMID : 0603520020070030161
Abstract
Gradual loss of telomere ends limits the growth capacity of primary cells whereas telomerase reactivation facilitates telomere maintenance and immortal cell growth in over 85% of human cancers. While telomerase activity is not detectable in most human somatic cells, inhibition of telomerase activity is thought to be a potential target for anticancer therapies. Here we show that telomerase inhibition has a profound effect on cell growth in mouse embryonic fibroblasts (MEFs) derived from telomerase-deficient mice. Telomere dysfunction exemplified by the formation of chromosomal end-to-end fusions was found to be an important factor of the growth impairment in telomerase-deficient cells. Multi-chromosomal fusion after exposure to doxorubicin is a typical characteristic of chromosomal abnormality. These findings indicate that chromosomal end-to-end fusion is a critical factor for the impairment of cell growth in telomerase-deficient cells and multi-chromosomal fusion might be one mechanistic basis of doxorubicin in conjunction with telomere function.
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Telomerase;Telomere;Chromosomal end to fusion;Cell growth
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