Evidence map›Paper›PMID 36499558›Full record

ArticleInternational journal of molecular sciences2022

EPLIN, a Putative Tumour Suppressor in Colorectal Cancer, Implications in Drug Resistance.

Jianyuan Zeng, Andrew J Sanders, Lin Ye, Rachel Hargest, Fiona Ruge, Wen G Jiang

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

4 citing papers in PubMed, 8 citations in OpenAlex.

  1. Chaperonin in health and disease.Molecular biomedicine · 2026
    Review
  2. Article
  3. Article
  4. State-of-the-Art Molecular Oncology in UK.International journal of molecular sciences · 2023
    Article
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 2 institutions in 1 country.

Jianyuan ZengSchool of Medicine, Cardiff University, Henry Wellcome Building, Cardiff CF14 4XN, UK.ORCID 0000-0001-5759-9710
Andrew J SandersSchool of Medicine, Cardiff University, Henry Wellcome Building, Cardiff CF14 4XN, UK.
Lin YeSchool of Medicine, Cardiff University, Henry Wellcome Building, Cardiff CF14 4XN, UK.
Rachel HargestSchool of Medicine, Cardiff University, Henry Wellcome Building, Cardiff CF14 4XN, UK.
Fiona RugeSchool of Medicine, Cardiff University, Henry Wellcome Building, Cardiff CF14 4XN, UK.
Wen G JiangSchool of Medicine, Cardiff University, Henry Wellcome Building, Cardiff CF14 4XN, UK.ORCID 0000-0002-3283-1111
Cardiff University · GBUniversity of Gloucestershire · GB

Funding

RealCan Fellowship to AJS, Cardiff China Medical Scholarship to JZ NA
6 · The paper itself

Abstract

Colorectal cancer is a serious threat to human health. Poor prognosis and frequently reported drug resistance urges research into novel biomarkers and mechanisms to aid in the understanding of the development and progression of colorectal cancer and to optimise therapeutic strategies. In the current study, we investigated the roles of a putative tumour suppressor, EPLIN, in colorectal cancer. Our clinical colorectal cancer cohort and online databases revealed a downregulation of EPLIN in colorectal cancer tissues compared with normal tissues. The reduced expression of EPLIN was associated with poor clinical outcomes of patients. In vitro cellular function assays showed that EPLIN elicited an inhibitory effect on cellular growth, adhesion, migration and invasion. Utilising a protein microarray on protein samples from normal and tumour patient tissues suggested HSP60, Her2 and other signalling events were novel potential interacting partners of EPLIN. It was further revealed that EPLIN and HSP60 were negative regulators of Her2 in colorectal cancer cells. The clinical cohort also demonstrated that expression of HSP60 and Her2 affected clinical outcomes, but most interestingly the combination of EPLIN, HSP60 and Her2 was able to identify patients with the most unfavourable clinical outcome by independently predicting patient overall survival and disease free survival. Furthermore, EPLIN and HSP60 exhibited potential to regulate cellular response to chemotherapeutic and EGFR/Her2 targeted therapeutic agents. In conclusion, EPLIN is an important prognostic factor for patients with colon cancer and reduced EPLIN in CRC contributes to aggressive traits of CRC cells and their responses to chemotherapeutic drugs. Collectively, EPLIN is a pivotal factor for the development and progression of colorectal cancer and has important clinical and therapeutic values in this cancer type.

Indexed as

Colorectal NeoplasmsCytoskeletal ProteinsDown-RegulationDrug ResistanceHumansSignal TransductionCytoskeletal Proteinscolorectal cancerdrug resistanceEPLINHer2HSP60

Identifiers

PMID36499558
PMCPMC9736569
OpenAlexW4310675865

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.