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Comparison of gene expression changes in AML cells after SMARCA4, SMARCD2 or DPF2 knock-down

ABSTRACT: We explored the role of SMARCA4 and the two Brahma associated factors SMARCD2 and DPF2 in leukaemia. We observed the selective requirement for these factors for leukemic cell expansion, as well as extended survival of mice transplanted with leukaemic cells with reduced expression of these genes. Gene expression profiling revealed largely similar alterations with the down-regulation of each of these three factors, suggesting a concerted function in transformed blood cells. These changes included loss of pluripotency-associated signature but did not correlate with c-MYC down-regulation. Human acute monocytic leukemia cells (THP-1, ACC 16) were lentivirally transduced with pLKO-puro vectors carrying shRNAs against SMARCA4, SMARCD2 or DPF2. As a negative control, THP-1 cells were transduced with pLKO-puro-shScr (Scrambled). All samples were prepared as biological triplicates.

ORGANISM(S): Homo sapiens

SUBMITTER: Kristian Helin

PROVIDER: E-GEOD-67923 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Comparison of gene expression changes in AML cells after SMARCA4, SMARCD2 or DPF2 knock-down

Project description:We explored the role of SMARCA4 and the two Brahma associated factors SMARCD2 and DPF2 in leukaemia. We observed the selective requirement for these factors for leukemic cell expansion, as well as extended survival of mice transplanted with leukaemic cells with reduced expression of these genes. Gene expression profiling revealed largely similar alterations with the down-regulation of each of these three factors, suggesting a concerted function in transformed blood cells. These changes included loss of pluripotency-associated signature but did not correlate with c-MYC down-regulation.

2015-07-12 | GSE67923 | GEO

Knock down of C11orf67 by shRNA in SUM52PE

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Project description:Dpf2 is a subunit of the BAF/pBAF chromatin remodelling complex. We have used cross-linking affinity purification-mass spectrometry to explore Dpf2 protein interactions in mouse embryonic stem cells.

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Project description:Differential expression of mRNA were conducted in neuroblastoma cell line SKNDZ, which successfully transduced human miR-125b MYCN-amplification SKNDZ neuroblastoma cell line was transduced with MIRN125B2 gene with lentiviral vector (pLKO.1-puro), and selected by puromycin for 48 hours. Then the total RNA was extracted and analyzed the differential expression of a total of 29,187 genes by Oligonucleotide DNA microarray.

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Project description:Lysine lactylation (Kla) is a new type of histone mark implicated in the regulation of various functional processes such as transcription. However, how this histone mark acts in cancers remains unexplored due in part to a lack of knowledge about its reader proteins. Here, we observe that cervical cancer (CC) cells undergo metabolic reprogram by which lactate accumulation and thereby boost histone lactylation, particularly H3K14la. Utilizing a multivalent photoaffinity probe in combination with quantitative proteomics approach, we identify DPF2 as a candidate target of H3K14la. Biochemical studies as well as CUT&Tag analysis reveal that DPF2 is capable of binding to H3K14la, and co-localizes with it on promoters of oncogenic genes. Notably, disrupting the association between DPF2 and histone lactylation through structure-guided mutation blunts those cancer-related gene expression along with cell survival. Together, our findings reveal DPF2 as a bona fide H3K14la effector that couples histone lactylation to gene transcription and cell survival, offering insight into how histone Kla engages in transcription and tumorigenesis.

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DPF2 reads histone lactylation to drive transcription and tumorigenesis [RNA-seq]

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