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Human RBM33_HNSC_LC-MS/MS in project "RBM33 Acts as an m6A Reader Required for ALKBH5-mediated m6A Demethylation"

ABSTRACT: To identify the potential RBM33 interaction proteins, we established UM-SCC-1 cells stably expressing pCDH-Strep-Vec, or Strep-RBM33. After strep-tactin beads enrichment of RBM33 and its ascociated proteins, all the pull-downed proteins are subjected to LC-MS/MS analysis.

INSTRUMENT(S): LCQ Classic

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture, Keratinocyte

SUBMITTER: Fang Yu

LAB HEAD: Zhijian Qian

PROVIDER: PXD033861 | Pride | 2023-05-30

REPOSITORIES: Pride

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Dataset's files

Source:

			Action	DRS
	Coomassie_staining_gel.tif	Other
	Publication_Report_for_PM-859-search.xls	Xls
	RBM33-UM-SCC-1.sf3	Other
	Strep-RBM33.mgf	Mgf
	Strep-RBM33.raw	Raw

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RBM33 Acts as an m6A Reader Essential for ALKBH5-mediated m6A Demethylation and Head and Neck Squamous Carcinoma Tumorigenesis [m6A-seq]

Project description:Head and neck squamous cell carcinoma (HNSC) is one of the most common malignant cancers worldwide. However, it is always detected at an advanced stage because of a lack of biomarkers for early diagnosis. Here, we identify the RNA binding motif protein 33 (RBM33) is commonly up-regulated in HNSC and it is essential for tumorigenesis. Mechanistically, RBM33 is an m6A reader protein and forms a complex with ALKBH5. RBM33 plays crucial roles in ALKBH5-mediated mRNA m6A demethylation not only by recruitment ALKBH5 to substrate but also activation its demethylase activity through inhibition it’s SUMOylation. Moreover, global transcriptomic and epitranscriptomic analyses identify that DDIT4 is a functional downstream target gene for RBM33 in HNSC and RBM33-mediated HNSC tumorigenesis by inhibition the mTOR pathway through the inhibition of m6A-dependent DDIT4 mRNA decay. Taken together, our study uncovers a novel molecular mechanism that RBM33/ALKBH5/m6A/DDIT4/mTOR axis regulates HNSC progression through the inhibition of mTOR pathway and targeting RBM33 may be a promising strategy for HNSC treatment.

2023-09-05 | GSE242276 | GEO

RBM33 Acts as an m6A Reader Essential for ALKBH5-mediated m6A Demethylation and Head and Neck Squamous Carcinoma Tumorigenesis

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Genetic aberrations in MAP kinase pathway play an important role in erlotinib resistance in head and neck cancer

Project description:Epidermal growth factor receptor (EGFR), a receptor tyrosine kinase is overexpressed in 90% of Head and neck squamous cell carcinoma (HNSCC) patients. Clinical trials with EGFR-targeted tyrosine kinase inhibitors such as erlotinib have shown a modest activity in HNSCC alternate mechanisms of resistance are acquired. To investigate these acquired mechanisms of resistance and identify novel therapeutic targets we employed whole exome sequencing of an isogenic pair of erlotinib sensitive (SCC-S) and resistant (SCC-R) HNSCC cell line. We observed single nucleotide variations and copy number alterations in genes related to RAS-RAF-MEK-ERK pathway. To assess the effects of these variations on cellular kinome and we employed SILAC-based phosphoproteomic analysis of SCC-S and SCC-R cell lines. Quantitative phosphoprotein profiling led to identification of 5558 unique phosphopeptides and 5025 unique phosphosites corresponding to 2344 proteins. We observed, 903 phosphopeptides belonging to 579 proteins and 518 phosphopeptides belonging to 368 proteins to be hyper and hypophosphorylated (≥2 fold) in SCC-R cells, respectively. Bioinformatics analysis of differentially phosphorylated proteins showed enrichment of proteins involved in MAPK pathway downstream of EGFR. We identified and validated activation of proteins related to MAPK pathway and its downstream targets in SCC-R cells. We further demonstrated that MAP2K1 inhibitor can be used as an alternative to erlotinib in HNSCC.

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miRNA expression profiling in squamous cell carcinoma (SCC)

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SILAC-based proteomic approach to delineate molecular alterations associated with erlotinib resistance in head and neck squamous cell carcinoma

Project description:Although Epidermal growth factor receptor (EGFR) is overexpressed in 90% of Head and neck squamous cell carcinoma (HNSCC) patients. Clinical trials with EGFR-targeted small molecule inhibitors such as erlotinib have shown a modest activity in recurrent or advanced HNSCC. To investigate the acquired mechanisms of erlotinib resistance we employed SILAC-based total proteomic analysis of an isogenic pair of erlotinib sensitive (SCC-S) and resistant (SCC-R) HNSCC cell line. This resulted in the identification of 5,427 proteins of which 532 proteins were overexpressed and 527 proteins were downregulated in SCC-R cells as compared to SCC-S cells (≥2 fold). Several proteins known to mediate erlotinib resistance in HNSCC and lung cancer were found to be dysregulated. Bioinformatics analysis of differentially expressed proteins showed enrichment of proteins involved in focal adhesion kinase (FAK) pathway downstream of EGFR. We identified CUB-domain containing protein 1 (CDCP1) and integrin β1 as upstream regulators of FAK signalling pathway to be overexpressed. We further demonstrated that CDCP1 and FAK can be targeted in combination as an alternative to erlotinib in HNSCC.

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RBM33 Acts as an m6A Reader Essential for ALKBH5-mediated m6A Demethylation and Head and Neck Squamous Carcinoma Tumorigenesis [PAR-CLIP]

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RBM33 Acts as an m6A Reader Essential for ALKBH5-mediated m6A Demethylation and Head and Neck Squamous Carcinoma Tumorigenesis [RIP-seq]

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