The C/EBPbeta isoform, liver-inhibitory protein (LIP), induces autophagy in breast cancer cell lines.
The C/EBPbeta isoform, liver-inhibitory protein (LIP), induces autophagy in breast cancer cell lines.
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DOI：
10.1016/j.yexcr.2010.07.021
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发表时间：
2010-11-15
影响因子：
3.7
通讯作者：
Sealy L
中科院分区：
文献类型：
--
作者：
Abreu MM;Sealy L
自噬是一个涉及细胞质中细胞成分通过溶酶体降解途径大量降解的过程。自噬在营养或生长因子耗尽等应激条件下表现出保护作用；然而，生存所必需的调节分子或细胞器的广泛降解可能导致细胞死亡或自噬介导的细胞死亡。自噬在癌症中的作用很复杂，在肿瘤抑制和肿瘤促进中都有作用。在这里，我们报道了 C/EBPbeta 转录因子的同种型，即肝脏富集抑制蛋白 (LIP)，可诱导人类乳腺癌细胞死亡并刺激自噬。 LIP 的过度表达与细胞生长不相容，并且当进行细胞周期分析时，没有观察到经历凋亡的细胞的 DNA 谱。相反，当通过电子显微镜检查时，表达 LIP 的细胞似乎具有大的自噬囊泡。通过监测酸性囊泡细胞器的发育和 LC3 从细胞质形式到膜结合形式的转化，进一步评估了 LIP 表达细胞的自噬。我们的工作表明，C/EBPbeta 同种型 LIP 是转录因子组的另一个成员，包括 E2F1 和 p53，它们能够在自噬中发挥作用。
Autophagy is a process involving the bulk degradation of cellular components in the cytoplasm via the lysosomal degradation pathway. Autophagy manifests a protective role in stressful conditions such as nutrient or growth factor depletion; however, extensive degradation of regulatory molecules or organelles essential for survival can lead to the demise of the cell, or autophagy-mediated cell death. The role of autophagy in cancer is complex with roles in both tumor suppression and tumor promotion proposed. Here we report that an isoform of the C/EBPbeta transcription factor, liver-enriched inhibitory protein (LIP), induces cell death in human breast cancer cells and stimulates autophagy. Overexpression of LIP is incompatible with cell growth and when cell cycle analysis was performed, a DNA profile of cells undergoing apoptosis was not observed. Instead, LIP expressing cells appeared to have large autophagic vesicles when examined via electron microscopy. Autophagy was further assessed in LIP expressing cells by monitoring the development of acidic vesicular organelles and conversion of LC3 from the cytoplasmic form to the membrane-bound form. Our work shows that C/EBPbeta isoform, LIP, is another member of the group of transcription factors, including E2F1 and p53, which are capable of playing a role in autophagy.
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影响因子：
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