Evidence map›Paper›PMID 32321509›Full record

ArticleCell communication and signaling : CCS2020

Effect of CIP2A and its mechanism of action in the malignant biological behavior of colorectal cancer.

Wei Chen, Jing-Lin Liang, Kai Zhou, Qing-Li Zeng, Jun-Wen Ye, Mei-Jin Huang

Open access · goldAbstract readVideo-Audio Media
In one paragraph

Article in Cell communication and signaling : CCS, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. The Pivotal Role of Protein Phosphatase 2A (PP2A) in Brain Tumors.International journal of molecular sciences · 2022
    Review
  8. Article
  9. Article
  10. CIP2A regulates MYC translation (via its 5'UTR) in colorectal cancer.International journal of colorectal disease · 2021
    Article
  11. Review
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

6 authors at 4 institutions in 1 country.

Wei ChenDepartment of Colorectal Surgery, The Six Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510655, China.
Jing-Lin LiangDepartment of Colorectal Surgery, The Six Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510655, China.
Kai ZhouJiangxi Provincial People's Hospital, Nanchang, 330006, Jiangxi, China.
Qing-Li ZengJiangxi Provincial People's Hospital, Nanchang, 330006, Jiangxi, China.
Jun-Wen YeDepartment of Colorectal Surgery, The Six Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510655, China.
Mei-Jin HuangDepartment of Colorectal Surgery, The Six Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510655, China. 13924073322@139.com.
Sixth Affiliated Hospital of Sun Yat-sen University · CNSun Yat-sen University · CNFirst Affiliated Hospital of Nanchang University · CNJiangxi Provincial People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIncreasing evidence has revealed a close correlation between cancerous inhibitor of protein phosphatase 2A (CIP2A) and cancer progression. CIP2A has been shown to participate in diverse biological processes, such as development, tumorigenic transformation and chemoresistance. However, the functions of CIP2A in colorectal cancer (CRC) and its underlying mechanisms of action are not yet completely understood. The purpose of this study was to explore its clinical significance, function and relevant pathways in CRC.

methodsQuantitative RT-PCR (qRT-PCR), immunohistochemistry (IHC), western blotting and enzyme-linked immunosorbent assay (ELISA) were used to identify the expression of CIP2A in CRC tissues, sera and CRC cell lines. The association between the expressions of CIP2A and patient survival was analyzed using the Kaplan-Meier curves. Additionally, the functional role of CIP2A in the cell lines was identified through small interfering RNA (siRNA)-mediated depletion of the protein followed by analyses of proliferation and xenograft growth in vivo using short hairpin (sh) RNAs. Effects of the C-myc inhibitor 10,058-F4 on the expressions of C-myc, and CIP2A in CRC cell lines and its potential mechanisms of action were investigated. Finally, the potential molecular pathways associated with CIP2A were screened using the phosphokinase array and identified through western blotting.

resultsCIP2A mRNA and protein levels were upregulated in CRC tissues compared to those of the corresponding normal tissues. It can be used as an independent prognostic indicator to determine overall survival (OS) and disease-free survival (DFS). Depletion of CIP2A substantially suppressed the growth of CRC cells and colony formation in vitro, and inhibited the growth of xenograft tumors in vivo. Additionally, the levels of CIP2A in the sera of patients with CRC were higher than those of the control subjects. Multivariate analyses revealed that the levels of CIP2A in the sera were not independent prognostic indicators in patients with CRC. Moreover, 10,058-F4 could effectively inhibit the growth of CRC cells in vitro, which could be correlated with an inhibition in the expressions of C-myc, CIP2A and its downstream regulatory anti-apoptotic proteins. Furthermore, the Human Phosphokinase Antibody Array was used to gain insights into the CIP2A-dependent intermediary signaling pathways. The results revealed that several signaling pathways were affected and the protein levels of p-p53 (S392), p-STAT5a (Y694), Cyclin D1, p-ERK1/2 and p-AKT (T308) had decreased in CIP2A-shRNA group based on the results of the western blot analysis.

conclusionsCIP2A could promote the development of CRC cells and predict poor prognosis in patients with CRC, suggesting that it may serve as a potential prognostic marker and therapeutic target against CRC. Video Abstract.

Indexed as

Colorectal NeoplasmsAnimalsAutoantigensBiomarkers, TumorCell Line, TumorCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansIntracellular Signaling Peptides and ProteinsMaleMembrane ProteinsMice, Inbred BALB CMiddle AgedTreatment OutcomeAutoantigensBiomarkers, TumorCIP2A protein, humanIntracellular Signaling Peptides and ProteinsMembrane Proteins10,058-F4Cell proliferationCIP2AColorectal cancerSerum

Identifiers

PMID32321509
PMCPMC7178757
OpenAlexW3020785513

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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.