Anoikis (detachment‐induced cell death) is a specific type of programmed cell death which occurs in response to the loss of the correct extracellular matrix connections. Anoikis resistance is an important mechanism in cancer invasiveness and metastatic behavior. Autophagy, on the other hand, involves the degradation of damaged organelles and the recycling of misfolded proteins and intracellular components. However, the intersection of these two cellular responses in lung cancer cells has not been extensively studied. Here, we identified that upon matrix deprivation, the lymphocyte lineage‐specific Ets transcription factor SPIB was activated and directly enhanced SNAP47 transcription in certain lung cancer cells. Loss of attachment‐induced autophagy significantly increased anoikis resistance by SPIB activation. Consistent with this function, SPIB depletion by short hairpin RNA abrogated SNAP47 transcriptional activation upon matrix deprivation. Therefore, these data delineate an important role of SPIB in autophagy‐mediated anoikis resistance in lung cancer cells. Accordingly, these findings suggest that manipulating SPIB‐regulated pathways in vivo and evaluating the impact of anoikis resistance warrant further investigation.

中文翻译：

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SPIB通过提高肺癌细胞中的自身溶酶体过程来促进无神经耐药性。

失语症（脱离引起的细胞死亡）是程序化细胞死亡的一种特殊类型，它是对正确的细胞外基质连接丢失的反应。厌食症的抵抗是癌症侵袭和转移行为的重要机制。另一方面，自噬涉及受损细胞器的降解以及错误折叠的蛋白质和细胞内成分的回收。但是，尚未广泛研究肺癌细胞中这两种细胞反应的交叉。在这里，我们发现基质被剥夺后，淋巴细胞谱系特异性的Ets转录因子SPIB被激活并直接增强了SNAP47在某些肺癌细胞中转录。附着诱导的自噬的丧失通过SPIB激活显着增加了对厌食症的抵抗力。与此功能一致，短发夹RNA的SPIB消耗在基质剥夺后废除了SNAP47转录激活。因此，这些数据描述了SPIB在肺癌细胞中自噬介导的失衡抗性中的重要作用。因此，这些发现表明，在体内操纵SPIB调节的途径并评估对厌氧症的抵抗性的影响值得进一步研究。