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。617Please respect copyright.ＰＥＮＡＮＡNtYIWzWXTk
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三十秒科學–腫瘤的周遭環境617Please respect copyright.ＰＥＮＡＮＡiV8gX3DbBy
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三十秒科學–癌細胞嗜糖的原因617Please respect copyright.ＰＥＮＡＮＡKdzFox9JFu
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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。617Please respect copyright.ＰＥＮＡＮＡF4rjdQFNuw
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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。617Please respect copyright.ＰＥＮＡＮＡQUpn0vBBov
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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)。617Please respect copyright.ＰＥＮＡＮＡWPUUt4gwzb
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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。617Please respect copyright.ＰＥＮＡＮＡnt3JB5FFG8
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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。617Please respect copyright.ＰＥＮＡＮＡc7sogZDNK6
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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。617Please respect copyright.ＰＥＮＡＮＡ4PcwmyFLGk
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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。617Please respect copyright.ＰＥＮＡＮＡFHvrqFFa0m
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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。617Please respect copyright.ＰＥＮＡＮＡPdpU8tZFA5
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。617Please respect copyright.ＰＥＮＡＮＡ3CkclFsfG7
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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。617Please respect copyright.ＰＥＮＡＮＡWlbQtOtp2x
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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。617Please respect copyright.ＰＥＮＡＮＡ89eKqrlnU5
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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。617Please respect copyright.ＰＥＮＡＮＡ60Xle7T79v
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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。617Please respect copyright.ＰＥＮＡＮＡ0REH7xFcKe
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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。617Please respect copyright.ＰＥＮＡＮＡteHfkaumGB
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如果想我快啲出文的話，請入去Penana網站科普專欄–薯不揀單俾一個like以及Bookmark，這對我非常之重要。617Please respect copyright.ＰＥＮＡＮＡ3q9hDOmCyN
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Ref1:https://pubmed.ncbi.nlm.nih.gov/8538748/617Please respect copyright.ＰＥＮＡＮＡNgduvFzxUo
