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SPIB promotes anoikis resistance via elevated autolysosomal process in lung cancer cells
Author(s) -
Zhang Hua,
Wang Guobin,
Zhou Ruimin,
Li Xiaobo,
Sun Yanan,
Li Yanzhe,
Du Wei,
Yan Xiaojie,
Yang Jie,
Chang Xinzhong,
Liu Zhe,
Ma Zhenyi
Publication year - 2020
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/febs.15272
Subject(s) - anoikis , transcription factor , biology , microbiology and biotechnology , programmed cell death , cancer research , autophagy , cancer cell , cancer , genetics , apoptosis , gene
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. Database RNA sequencing and ChIP sequencing data are available in Gene Expression Omnibus database under the accession numbers GSE106592 and GSE125561 , respectively.