IL-2诱导宫颈癌细胞凋亡,增加细胞色素c的产生和表达,抑制COX IV

E. I. Torres-Corioriles, I. D. Río-Ortiz, B. Weiss-Steider, M. Barrios-Maya, Leonardo Trujullo-Cirilo, T. Corona-Ortega, R. Rangel-Corona
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摘要

已知宫颈癌细胞表达IL-2受体(IL-2R),高剂量可诱导细胞死亡。用100 IU/ml IL-2培养宫颈癌细胞株CALO和INBL,以鉴定细胞死亡类型。我们的研究结果表明,细胞膜外表面磷脂酰丝氨酸的显著表达、典型的DNA片段的存在和caspase 3的激活是凋亡细胞死亡的存在。我们还观察到COX I、COX II和COX III的表达没有明显改变,而COX IV的表达完全被抑制。共聚焦显微镜观察到细胞色素c的表达增加。最后,我们推测IL-2用于癌症治疗的临床效果和毒性主要是由于其对癌细胞本身的凋亡作用,而不是像以前认为的那样,是白细胞的细胞毒性作用。
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IL-2 induces apoptosis, increases the production and expression of cytochrome-C and inhibits COX IV in cervical cancer cells
It is known that cervical cancer cells express IL-2 receptor (IL-2R) and those high doses induce cell death. To identify the type of cell death two cervical cancer cell lines, CALO and INBL, were cultured with 100 IU/ml of IL-2. Our results showed the presence of apoptotic cell death by the significant expression of phosphatidylserine on the external surface of cellular membranes, the presence of a typical DNA fragmentation and the activation of caspase 3. We also observed that the expression of COX I, COX II and COX III was not significantly altered while that of COX IV was completely inhibited. An increased expression of cytochrome-C by confocal microscopy was observed. Finally, we speculate that the clinical effect and toxicities of IL-2 used in cancer therapies is mostly due to its apoptotic effect on the cancer cells themselves rather than, as thought, the cytotoxic contribution of leukocytes.
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