Proteomics

Dataset Information

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Mutant p53, mutant KRAS and hyperactive CMYC downstream proteomic programs in lung, colon and pancreatic cancer cell lines

ABSTRACT: Human cancer cell lines indicated in the file names, with stably overexpressed Cas9 nuclease, were transfected with (C) control sgRNA or (P) TP53-specific sgRNA, (K) KRAS-specific sgRNA or (M) CMYC-specific sgRNA. Each experiment was done by transfection of sgRNA pair - control (C) or causing a NHEJ-mediated knock-out of the target genes (P, K or M). Samples for proteomics were collected 48h post sgRNA transfection without selection, in three biological replicates each (indicated with numbers 1-3). In cell lines with three activated oncogenes, three separate oncogene-targeting transfections were carried out.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture

SUBMITTER: Jacek Wisniewski  

LAB HEAD: Jacek R Wisniewski

PROVIDER: PXD037398 | Pride | 2024-10-17

REPOSITORIES: Pride

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20191113_QX8_JRW_SA_L_SS10.raw Raw
20191113_QX8_JRW_SA_L_SS11.raw Raw
20191113_QX8_JRW_SA_L_SS12.raw Raw
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Publications

A common druggable signature of oncogenic c-Myc, mutant KRAS and mutant p53 reveals functional redundancy and competition among oncogenes in cancer.

Grześ Maria M   Jaiswar Akanksha A   Grochowski Marcin M   Wojtyś Weronika W   Kaźmierczak Wojciech W   Olesiński Tomasz T   Lenarcik Małgorzata M   Nowak-Niezgoda Magdalena M   Kołos Małgorzata M   Canarutto Giulia G   Piazza Silvano S   Wiśniewski Jacek R JR   Walerych Dawid D  

Cell death & disease 20240831 8

The major driver oncogenes MYC, mutant KRAS, and mutant TP53 often coexist and cooperate to promote human neoplasia, which results in anticancer therapeutic opportunities within their downstream molecular programs. However, little research has been conducted on whether redundancy and competition among oncogenes affect their programs and ability to drive neoplasia. By CRISPR‒Cas9-mediated downregulation we evaluated the downstream proteomics and transcriptomics programs of MYC, mutant KRAS, and m  ...[more]

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