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SNHG29 knockdown by CRISPRi and shRNA in M07e acute myeloid leukemia cells

ABSTRACT: The long non-coding RNA SNHG29 has been identified as a candidate essential gene in acute myeloid leukemia (AML) through a genome-wide CRISPRi depletion screen. To characterize the transcriptomic consequences of SNHG29 loss, we performed RNA-seq in M07e AML cells following SNHG29 knockdown using two independent methods: CRISPRi (two sgRNAs targeting the SNHG29 promoter, with Luciferase-targeting sgRNA as control) and shRNA (two shRNAs targeting SNHG29, with scrambled shRNA as control). Three biological replicates were generated per condition. Differential expression analysis was performed using DESeq2.

ORGANISM(S): Homo sapiens

PROVIDER: GSE326774 | GEO | 2026/06/30

REPOSITORIES: GEO

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Project description:In the recent years, massively parallel sequencing approaches identified hundreds of mutated genes in cancer providing an unprecedented amount of information about mechanisms of cancer cell maintenance and progression. However, while (it is widely accepted that) transformation processes result from oncogenic cooperation between deregulated genes and pathways, the functional characterization of candidate key players is mostly performed at the single gene level which is generally inadequate to identify these oncogene circuitries. In addition, studies aimed at depicting oncogenic cooperation involve the generation of challenging mouse models or the deployment of tedious screening pipelines. Genome wide mapping of epigenomic modifications on histone tails or binding of factors such as MED1 and BRD4 allowed identification of clusters of regulatory elements, also termed Super-Enhancers (SE). Functional annotation of these regions revealed their high relevance during normal tissue development and cancer ontogeny. An interesting paradigm of the tumorigenic function of these SE regions comes from ETO2-GLIS2-driven acute megakaryoblastic leukemia (AMKL) in which the fusion protein ETO2-GLIS2 is sufficient to promote an aberrant transcriptional network by the rewiring of SE regions4. We thus hypothesized that important regulatory regions could control simultaneously expression of genes cooperating in functional modules to promote cancer development. In an effort to identify such modules, we deployed a genome-wide CRISPRi-based screening approach and nominated SE regions that are functionally linked to leukemia maintenance. In particular, we pinpointed a novel SE region regulating the expression of both tyrosine kinases KIT and PDGFRA. Whereas the inhibition of each kinase alone affected modestly cancer cell growth, combined inhibition of both receptors synergizes to impair leukemia cell growth and survival. Our results demonstrate that genome-wide screening of regulatory DNA elements can identify co-regulated genes collaborating to promote cancer and could open new avenues to the concept of combined gene inhibition upon single hit targeting.

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SNHG29 knockdown by CRISPRi and shRNA in M07e acute myeloid leukemia cells

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