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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2002.1
- 수록면
- 3 - 113 (111page)
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Transformation with viral oncogene extends thelifespan of normal cells beyond replicative senes-cence called M1, but most of them eventually suc-cumb to second crisis called M2 when telomeresbecome critically short. To acquire an infinite growthcapacity, these cells have to overcome M2 crisis,which is known to follow telomerase activation. Wehave investigated if telomerase expression isrequired for virus-transformed pre-M2 cells to avertM2 crisis. Human retinal pigment epithelial (RPE)cells were transformed with simian virus 40 large Tantigen and a VR3 clone in pre-M2 stage wasobtained. Then, VR3 cells were transfected with atelomerase-containing vector and two cell lines thatexpressed telomerase temporarily or continuouslywere cloned and designated as ST1 and ST2,respectively. Normal RPE cells went into senes-cence after 36 population doublings. Although thelifespan was extended in the VR3 clone about 20times more, it eventually underwent second crisis.The telomere length of VR3 decreased compared tothat of normal RPE cells and the decrease continuedduring subculture. However, the ST1 and ST2 clonesthat expressed both T antigen and telomerase couldavert this crisis. The initial telomere length of ST1and ST2 was longer than that of normal cells. TheST1 underwent growth arrest again as telomeraseexpression faded out and elongated telomere wasshortened, but the ST2 that maintained telomeraseactivity and telomere length proliferated continu-ously. In conclusion, telomerase activation is defi-nitely required to overcome M2 crisis and acquire aninfinite lifespan in human somatic epithelial cellsand this mechanism is independent from M1 crisescape in cell immortalization.
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