Dataset Information

Mass spectrometry analysis for IP with NEIL1 Antibody in CRC DLD-1 cell

ABSTRACT: NEIL1 overexpression was performed in CRC DLD-1 cells. The protein interacted with NEIL1 were analyzed by Mass spectrometry. The NEIL1 overexpressed and control cells in the logarithmic growth phase were collected for IP with NEIL1 Antibody.

ORGANISM(S): Homo Sapiens

SUBMITTER: Fengwei Wang

PROVIDER: PXD040878 | iProX | Wed Mar 15 00:00:00 GMT 2023

REPOSITORIES: iProX

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Publications

NEIL1 drives the initiation of colorectal cancer through transcriptional regulation of COL17A1.

Cao Jing-Hua JH Cao Chen-Hui CH Lin Jin-Long JL Li Si-Yu SY He Long-Jun LJ Han Kai K Chen Jie-Wei JW Li Si S Wang Xin X Xie Dan D Wang Feng-Wei FW

Cell reports 20240103 1

Deficiency of DNA repair pathways drives the development of colorectal cancer. However, the role of the base excision repair (BER) pathway in colorectal cancer initiation remains unclear. This study shows that Nei-like DNA glycosylase 1 (NEIL1) is highly expressed in colorectal cancer (CRC) tissues and associated with poorer clinical outcomes. Knocking out neil1 in mice markedly suppresses tumorigenesis and enhances infiltration of CD8<sup>+</sup> T cells in intestinal tumors. Furthermore, NEIL1 ...[more]

PMID: 38175757

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Project description:Colorectal cancer (CRC) is the third most deadly and fourth most diagnosed cancer worldwide. Despite the progress in early diagnosis and advanced therapeutic options, CRC shows a poor prognosis with a 5-year survival rate of ~45%. PRDM2/RIZ, a member of Positive Regulatory Domain (PRDM) gene family, expresses two main molecular variants, the PR-plus isoform (RIZ1) and the PR-minus (RIZ2). The imbalance in their expression levels in favour of RIZ2 is observed in many cancer types. The full length RIZ1 has been extensively investigated in several cancers where it acts as a tumour suppressor, whereas few studies have explored the RIZ2 oncogenic properties. PRDM2 is often target of frameshift mutations and aberrant DNA methylation in CRC. Accordingly, our analysis of Exome- and transcriptome public datasets available at The Cancer Genome Atlas (TCGA) portal revealed that PRDM2 gene is frequently mutated and transcriptionally deregulated in CRC. However, little is known about its role in CRC. In this study, we first evaluated the expression of the different PRDM2 transcripts by in silico analysis on TCGA CRC datasets. Our in-silico analysis on TCGA datasets revealed a highly significant downregulation of RIZ1 in CRC samples whereas a RIZ2 increase was observed in the same samples. Then, we assayed several CRC cell lines by qRT-PCR analysis for the main PRDM2 transcripts and selected DLD-1 cell line, which showed the lowest RIZ2 levels to mimic TCGA datasets analysis results and consequently to assess the PRDM2/RIZ2 role in CRC cells. RNAseq analysis revealed that RIZ2 overexpression induced an EGF overexpression suggesting that RIZ2 could be involved in the EGF autocrine regulation of DLD-1 cell behaviour. Noteworthy, the forced RIZ2 expression increased cell viability, growth, colony formation, migration and organoid formation thus confirming our previous findings on HEK-293 cells. These effects could be mediated by the release of high EGF levels by RIZ2 overexpressing DLD-1 cells. Our findings add novel insights on the putative RIZ2 tumor-promoting functions in CRC, although additional attempts are warranted to depict the underlying molecular mechanism of action

Dataset Information

Mass spectrometry analysis for IP with NEIL1 Antibody in CRC DLD-1 cell

Publications

NEIL1 drives the initiation of colorectal cancer through transcriptional regulation of COL17A1.

Similar Datasets

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