Proteomics

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Proteomics analysis for RBM17 in acute myeloid leukemia

ABSTRACT: Acute myeloid leukemia (AML) patients suffer from chemo-resistance, high relapse frequency, and low overall survival rate, outcomes driven by leukemic stem cells (LSCs). Understanding the molecular mechanisms that support these primitive leukemic cells is crucial for developing effective AML therapeutics. In the present study, we demonstrate that upregulation of the splicing factor RBM17 preferentially marks and sustains the primitive compartment of AML. We performed shotgun proteomics to characterize the proteome changes upon RBM17 knockdown in AMl cells. In addition, we used proteomics to analyze the proteome changes after knockdown of EIF4A2, a direct splicing substrate of RBM17 in AML cells.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Leukocyte, Cell Culture

DISEASE(S): Acute Leukemia

SUBMITTER: Yu Lu  

LAB HEAD: Yu Lu

PROVIDER: PXD026780 | Pride | 2022-08-12

REPOSITORIES: Pride

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20200102-Lina-K562-RBM17KD-Day5-TMT6-40ug-36cut-F01.raw Raw
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Publications

The splicing factor RBM17 drives leukemic stem cell maintenance by evading nonsense-mediated decay of pro-leukemic factors.

Liu Lina L   Vujovic Ana A   Deshpande Nandan P NP   Sathe Shashank S   Anande Govardhan G   Chen He Tian Tony HTT   Xu Joshua J   Minden Mark D MD   Yeo Gene W GW   Unnikrishnan Ashwin A   Hope Kristin J KJ   Lu Yu Y  

Nature communications 20220704 1

Chemo-resistance in acute myeloid leukemia (AML) patients is driven by leukemic stem cells (LSCs) resulting in high rates of relapse and low overall survival. Here, we demonstrate that upregulation of the splicing factor, RBM17 preferentially marks and sustains LSCs and directly correlates with shorten patient survival. RBM17 knockdown in primary AML cells leads to myeloid differentiation and impaired colony formation and in vivo engraftment. Integrative multi-omics analyses show that RBM17 repr  ...[more]

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