종양괴사인자(TNF)가 ME-180 사람 경부 암종세포에서 종양 발생 유전자의 발현에 미치는 영향

• 영문명: Effect of Tumor Necrosis Factor-alpha(TNF) on the Expression of Oncogenes in ME-180 Human Cervical Carcinoma Cells
• 발행기관: 대한약학회
• 저자명: 한형미(Hyung Mee Han) 김형수(Hyung Soo Kim) 손경희(Kyung Hee Sohn) 최경백(Kyoung Baek Choi) 정승태(Seung Tae Chung) 김진호(Jin Ho Kim) 이병무(Byung Moo Lee) 김주일(Joo Il Kim)
• 간행물 정보: 『약학회지』제41권 제5호 (1997년), 629~637쪽, 전체 9쪽
• 주제분류: 의약학 > 기타의약학
• 파일형태: PDF
• 발행일자: 1997.10.31

영문 초록

Tumor necrosis factor-alpha (TNF) induced a cytotoxic response in ME-180 cervical carcinoma cells in vitro. This cytotoxic response was accompanied by a temporal series of mitogenic stimuli : increased c-fos, c-jun and jun-B expression. Depletion of protein kinase C (PKC) by exposure of ME-180 cells to 100ng/ml phorbol myristate acetate (PMA) for 24hours almost completely abolished TNF-mediated increase in these signals, indicating that a PKC-dependent pathway is involved in TNF-mediated increases in the expression of c-fos, c-jun and jun-B. Characteristics of TNF receptors after exposure to 100ng/ml PMA or 24hours were not altered, suggesting that diminished induction of these oncogenes by TNF after PMA treatment is not due to any changes at the receptor level. To examine whether a PKC-dependent pathway is involved in TNF-mediated cytotoxicity in ME-180 cells, cytotoxicity was measured after depletion of PKC. No apparent changes in cytototoxicity after PKC depletion suggest that a PKC-dependent pathway is not involved in TNF-mediated cytotoxicity. Furthermore, results from cytotoxicity tests after exposure to staurosporine (PKC inhibitor) did not show any changes in the TNF-mediated cytotoxicity, confirming that a PKC-dependent pathway is not involved in this process. These data indicate that 1) TNF induces expression of c-fos, c-jun and jun-B oncogenes via a PKC-dependent pathway and 2) PKC-dependent expression of these three oncogenes by TNF may not be involved in TNF-mediated cytotoxicity in ME-180 cells.

키워드

TNF-α oncogene expression protein kinase C cytotoxicity.