原癌基因串扰、反馈与表达与抗癌药物耐药

M. Elalfy, M. G. Elhadidy, E. M. El Nashar
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摘要

原癌基因如C-MYC、EGFR等在再生、伤口和任何应激性损伤中具有维持组织回声和愈合的生理功能。值得注意的是,这些生长因子共同作用,在组织重塑后,其寿命保持在基础水平,并保持其功能,就像部分肝切除术一样。而在癌症中,正如我们在肝癌的2个转基因模型中所做的那样,我们注意到致癌基因彼此不喜欢,只有其中一个是高度表达的,它使其他基因保持在基础水平或降解。此外,如果一个癌基因被抑制或沉默,其他癌基因就会变得活跃或表达,从而导致抗癌耐药。因此,双特异性抗体可以成功地降低抗癌药物的耐药性。
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Proto-oncogenes Crosstalk, Feedback and Expression, and Anticancer Drugs Resistance
Proto-oncogenes like C-MYC, EGFR and others have physiological function in regeneration, wound and any stressfully injury to maintain tissue echotexture and healing. Notably, these growth factors work together and had life span to retain to basal level after tissue remodeling and retain its function like what happen in partial hepatectomy. While in cancer, as we work out in 2 transgenic model of liver cancer, we notice that oncogenes do not like each other and just one of them was highly expressive, it keeps other ones at basal level or degraded. Moreover, if one oncogene was inhibited or silenced, other oncogenes become active or expressed and result in anticancer drug resistance. So bispecific antibody could successfully reduce anti-cancer drug resistance.
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