上兩集簡述了癌細胞缺氧的成因,以及缺氧導致癌細胞相對上更為依賴葡萄糖作新陳代謝用途。612Please respect copyright.PENANAYXzvME5Zbx612Please respect copyright.PENANAnoJrCtqJ0U
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三十秒科學–腫瘤的周遭環境612Please respect copyright.PENANAvhTJoHDEA6
https://lih.kg/gFPfPS612Please respect copyright.PENANAd4VvBDsTAg
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三十秒科學–癌細胞嗜糖的原因612Please respect copyright.PENANA7hYfZ8zsZr
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今集我們會講述缺氧對癌細胞自身發展的其中一道好處。612Please respect copyright.PENANAHKYOJAvvHR
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(圖2)當DNA出現異變的時候,細胞裡名為p53的蛋白質便會出手幫忙,號令細胞停止生長(Cell cycle arrest),給予時間讓其他蛋白質幫忙協助修復DNA。612Please respect copyright.PENANAgP20bU588H612Please respect copyright.PENANA6XJpC3VtXQ
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若果細胞最後還是無法處理修復DNA的工作,p53便會指示細胞趨向死亡程序(Apoptosis)。612Please respect copyright.PENANAhw6TZ6raRh
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腫瘤的出現,是無數DNA變異得出來的成果。因此在這方面來看,p53是防止癌細胞出現的好幫手,因為p53會確保細胞的DNA不會出現變異,或指令出現DNA變異的細胞消失。612Please respect copyright.PENANAoN3sq2GC0K
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但是,有一點非常矛盾的是,大部份普通細胞的p53蛋白質表達率非常低,它能否防止癌細胞出現這一點使人存疑。612Please respect copyright.PENANARHSeLAVt6t
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(圖3)事實上,非常諷刺的是,氧氣含量越低的話,P53蛋白質的表達率便會越高。612Please respect copyright.PENANA7vV6JiGJHS612Please respect copyright.PENANAtj2rUigqmt
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而在缺氧的環境下,擁有p53的蛋白質的細胞便會自動進行死亡。612Please respect copyright.PENANAzvrNEoA4cJ
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(圖4)重大的問題是,有部份缺氧的癌細胞會發展出變異版本的p53,失去原有的功能。612Please respect copyright.PENANAZDv2pX2rRV
在缺氧施加的壓力下,擁有正常p53版本的細胞會一一死去,變相幫忙篩選出擁有變異版本p53的細胞,使它們逐漸成為大多數。612Please respect copyright.PENANAuQUB5hH0lq612Please respect copyright.PENANAJXe5aic8OL
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而這些擁有變異版本p53的細胞,修復DNA的能力會大幅度被削弱,因而加劇了DNA變異速度,促成腫瘤繼續長大。612Please respect copyright.PENANAj3iUr5BAEF
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(圖5)圖中為腫瘤形成的其中一道概論,癌細胞自製的缺氧環境,變相提供了一道挑選擁有更強DNA變異能力細胞的環境。612Please respect copyright.PENANA9Qs2UWTyEB
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現實中大部分的的癌細胞均擁有p53變異,而擁有p53變異的細胞更具抵抗化療藥物cis-platin的能力。612Please respect copyright.PENANA09WZFx23HR
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除缺氧外,大陽的紫外光亦是促使p53變異的好幫手,不少皮膚癌細胞均出現至少一處的p53變異。612Please respect copyright.PENANApL0q2nKQa2
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那些不塗防曬便與陽光玩遊戲的人,一直是在玩命。612Please respect copyright.PENANAhRk88nzkv4
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Ref1:https://pubmed.ncbi.nlm.nih.gov/8538748/612Please respect copyright.PENANAHOqCJuMgVT