Evidence map›Paper›PMID 30850009›Full record

ArticleJournal of experimental & clinical cancer research : CR2019

Cysteine-rich intestinal protein 1 suppresses apoptosis and chemosensitivity to 5-fluorouracil in colorectal cancer through ubiquitin-mediated Fas degradation.

Lanzhi Zhang, Rui Zhou, Weibin Zhang, Xueqing Yao, Weidong Li, Lijun Xu, Xuegang Sun, Liang Zhao

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.4field-weighted citation impact, top 17% 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

27 citing papers in PubMed, 39 citations in OpenAlex.

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  20. Anti-Tumor Effects of Heat-KilledMicroorganisms · 2022
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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

8 authors at 4 institutions in 1 country.

Lanzhi ZhangDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, Guangdong, China.
Rui ZhouDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, Guangdong, China.
Weibin ZhangDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, Guangdong, China.
Xueqing YaoDepartment of General Surgery, Guangdong General Hospital, Guangdong Academy of Medical Science, Guangzhou, Guangdong, China.
Weidong LiDepartment of Medical Oncology, Affiliated Tumor Hospital of Guangzhou Medical University, Guangzhou, China.
Lijun XuDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, Guangdong, China.
Xuegang SunSchool of Traditional Chinese Medicine, Southern Medical University, Guangzhou, 510515, China. sxg_smu@126.com.
Liang ZhaoDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, Guangdong, China. liangsmu@foxmail.com.
Southern Medical University · CNGuangdong General Hospital · CNGuangzhou Medical University Cancer Hospital · CNNanfang Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCysteine-rich intestinal protein 1 (CRIP1) is highly expressed in human intestine and aberrantly expressed in several types of tumor. However, studies on CRIP1 are limited and its role on tumor development and progression remains controversial and elusive.

methodsImmunohistochemistry was performed to evaluate the expression of CRIP1 in paired normal and colorectal tumor specimens, as well as colorectal cell lines. Functional assays, such as CCK8, TUNEL assay and in vivo tumor growth assay, were used to detect the proliferation, apoptosis and response to 5-FU of CRIP1. Western blot was used to analyze Fas-mediated pathway induced by CRIP1. Rescue experiments were performed to evaluate the essential role of CRIP1 for Fas-mediated apoptosis.

resultsWe demonstrated that CRIP1 is overexpressed in CRC tissues compared with adjacent normal mucosa. CRIP1 could dramatically recover the 5-Fluorouracil (5-FU) inhibited CRC cell proliferation in vitro and stimulate the tumor formation of CRC in vivo, probably through inhibiting CRC cell apoptosis. Moreover, CRIP1 also dramatically recovered the 5-Fluorouracil (5-FU) induced tumor cell apoptosis in vitro. Further study demonstrated that CRIP1 down-regulated the expression of Fas protein and proteins related to Fas-mediated apoptosis. CRIP1 could interact with Fas protein and stimulate its ubiquitination and degradation. In addition, a negative correlation was detected between the expression of CRIP1 and Fas protein in most of the clinical human CRC samples.

conclusionThe current research reveals a vital role of CRIP1 in CRC progression, which provide a novel target for clinical drug resistance of colorectal cancer and undoubtedly contributing to the therapeutic strategies in CRC.

Indexed as

AnimalsApoptosisCarrier ProteinsCell Line, TumorCell ProliferationColorectal NeoplasmsDrug Resistance, Neoplasmfas ReceptorFluorouracilGene Expression Regulation, NeoplasticHumansLIM Domain ProteinsMiceMicroRNAsProteolysisUbiquitinCarrier ProteinsCRIP1 protein, humanFAS protein, humanfas ReceptorFluorouracilLIM Domain ProteinsMicroRNAsUbiquitinApoptosisChemoresistantColorectal cancerCysteine-rich intestinal protein 1FAS

Identifiers

PMID30850009
PMCPMC6408822
OpenAlexW2938357920

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Registered trials

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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.