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000182135 0247_ $$2doi$$a10.1016/j.canlet.2022.215958
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000182135 041__ $$aEnglish
000182135 082__ $$a570
000182135 1001_ $$0P:(DE-He78)1fc145734f64403c4ceeef52013b8bc1$$aMyacheva, Ksenia$$b0$$eFirst author$$udkfz
000182135 245__ $$aCRISPRi screening identifies CASP8AP2 as an essential viability factor in lung cancer controlling tumor cell death via the AP-1 pathway.
000182135 260__ $$aAmsterdam [u.a.]$$bElsevier Science$$c2023
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000182135 520__ $$aSince lung cancer remains the leading cause of cancer death globally, there is an urgent demand for novel therapeutic targets. We carried out a CRISPR interference (CRISPRi) loss-of-function screen for human lung adenocarcinoma (LUAD) targeting 2098 deregulated genes using a customized algorithm to comprehensively probe the functionality of every resolvable transcriptional start site (TSS). CASP8AP2 was identified as the only hit that significantly affected the viability of all eight screened LUAD cell lines while the viability of non-transformed lung cells was only moderately impacted. Knockdown (KD) of CASP8AP2 induced both autophagy and apoptotic cell death pathways. Systematic expression profiling linked the AP-1 transcription factor to the CASP8AP2 KD-induced cancer cell death. Furthermore, inhibition of AP-1 reverted the CASP8AP2 silencing-induced phenotype. Overall, the tailored CRISPRi screen profiled the impact of over 2000 genes on the survival of eight LUAD cell lines and identified the CASP8AP2 - AP-1 axis mediating lung cancer viability.
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000182135 650_7 $$2Other$$aAutophagy
000182135 650_7 $$2Other$$aCRISPR
000182135 650_7 $$2Other$$aCaspase
000182135 650_7 $$2Other$$aFLASH
000182135 650_7 $$2Other$$aLung adenocarcinoma
000182135 650_7 $$2Other$$aNSCLC
000182135 7001_ $$aWalsh, Andrew$$b1
000182135 7001_ $$0P:(DE-He78)2250d8065ae89ecda166ad1fa43b9262$$aRiester, Marisa$$b2$$udkfz
000182135 7001_ $$0P:(DE-HGF)0$$aPelos, Giulia$$b3
000182135 7001_ $$0P:(DE-HGF)0$$aCarl, Jane$$b4
000182135 7001_ $$0P:(DE-He78)93eb54ede184de6f9de29d827ffb27f6$$aDiederichs, Sven$$b5$$eLast author$$udkfz
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