蒙大拿州立大学研究团队发现了哺乳动物细胞的一个此前未知的生存机制1。这一发现表明，当传统的二硫化物还原酶系统失效时，细胞仍能通过备用通路制造必需氨基酸半胱氨酸1。研究成果已发表在《Nature Chemical Biology》期刊上1。
该备用通路通过断裂胱氨酸内相邻的碳硫键来释放半胱氨酸1。研究团队首次发现这一机制的线索始于2014年，当时基因工程小鼠在本应致命的条件下存活了下来1。科研人员用时九年才确定了这条备用通路的具体运作机制1。蒙大拿州立大学学生Zoe Seaford和Sydney Austad作为共同第一作者参与了研究1。
科研团队认为，这一细胞生存机制可能起源于早期多细胞生物对亲电毒素的防御1。该发现为理解癌细胞如何抵抗治疗提供了新视角，为通过阻断该通路增强肿瘤治疗效果指明了新方向1。
Researchers at Montana State University have identified a previously unknown survival mechanism in mammalian cells that allows them to produce the essential amino acid cysteine through an alternative pathway when the conventional disulfide reductase system fails.1 The discovery, published in Nature Chemical Biology, reveals how cells can circumvent what was thought to be a lethal condition, with potential applications in understanding cancer cell resistance to treatment.1
The alternate pathway functions by breaking carbon-sulfur bonds within cystine molecules to release cysteine.1 The research team, including Montana State University students Zoe Seaford and Sydney Austad as co-first authors, took nine years to determine the precise mechanism of this backup system.1 The initial observation occurred in 2014, when genetically engineered mice unexpectedly survived under conditions that should have been fatal.1 Scientists hypothesize that this cellular mechanism may have originated as an early defense strategy in multicellular organisms against electrophilic toxins.1 By understanding how cancer cells exploit such alternative survival pathways, researchers may develop new strategies to enhance tumor treatment effectiveness through pathway blockade.1
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