Evidence map›Paper›PMID 28181595›Full record

ArticleScientific reports2017

Comprehensive Proteomic Characterization of the Human Colorectal Carcinoma Reveals Signature Proteins and Perturbed Pathways.

Jian-Jiang Hao, Xiaofei Zhi, Yeming Wang, Zheng Zhang, Zeyu Hao, Rong Ye, Zhijie Tang, Fei Qian, Quhui Wang, Jianwei Zhu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

  1. Pooled it
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  8. Biomarker Identification through Proteomics in Colorectal Cancer.International journal of molecular sciences · 2024
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 2 countries.

Jian-Jiang HaoDepartment of Gastrointestinal Surgery, Affiliated Hospital of Nantong University, Nantong 226001, China.
Xiaofei ZhiDepartment of Gastrointestinal Surgery, Affiliated Hospital of Nantong University, Nantong 226001, China.
Yeming WangDepartment of Gastrointestinal Surgery, Affiliated Hospital of Nantong University, Nantong 226001, China.
Zheng ZhangPoochon Scientific, Frederick, Maryland 21701, USA.
Zeyu HaoWhiting School of Engineering of Johns Hopkins University, Baltimore, Maryland 21218, USA.
Rong YePoochon Scientific, Frederick, Maryland 21701, USA.
Zhijie TangDepartment of Gastrointestinal Surgery, Affiliated Hospital of Nantong University, Nantong 226001, China.
Fei QianDepartment of Gastrointestinal Surgery, Affiliated Hospital of Nantong University, Nantong 226001, China.
Quhui WangDepartment of Gastrointestinal Surgery, Affiliated Hospital of Nantong University, Nantong 226001, China.
Jianwei ZhuDepartment of Gastrointestinal Surgery, Affiliated Hospital of Nantong University, Nantong 226001, China.
Affiliated Hospital of Nantong University · CNNantong University · CNJohns Hopkins University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The global change in protein abundance in colorectal cancer (CRC) and its contribution to tumorigenesis have not been comprehensively analyzed. In this study, we conducted a comprehensive proteomic analysis of paired tumors and adjacent tissues (AT) using high-resolution Fourier-transform mass spectrometry and a novel algorithm of quantitative pathway analysis. 12380 proteins were identified and 740 proteins that presented a 4-fold change were considered a CRC proteomic signature. A significant pattern of changes in protein abundance was uncovered which consisted of an imbalance in protein abundance of inhibitory and activating regulators in key signal pathways, a significant elevation of proteins in chromatin modification, gene expression and DNA replication and damage repair, and a decreased expression of proteins responsible for core extracellular matrix architectures. Specifically, based on the relative abundance, we identified a panel of 11 proteins to distinguish CRC from AT. The protein that showed the greatest degree of overexpression in CRC compared to AT was Dipeptidase 1 (DPEP1). Knockdown of DPEP1 in SW480 and HCT116 cells significantly increased cell apoptosis and attenuated cell proliferation and invasion. Together, our results show one of largest dataset in CRC proteomic research and provide a molecular link from genomic abnormalities to the tumor phenotype.

Indexed as

ProteomeProteomicsSignal TransductionCell Line, TumorCell MovementCell ProliferationChromatinColorectal NeoplasmsGlycolysisHumansChromatinProteome

Identifiers

PMID28181595
PMCPMC5299448
OpenAlexW2587286943

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.