Evidence map›Paper›PMID 34422665›Full record

ArticleFrontiers in oncology2021

ARTEMIN Promotes Oncogenicity and Resistance to 5-Fluorouracil in Colorectal Carcinoma by p44/42 MAPK Dependent Expression of CDH2.

Qiu-Shi Zhuang, Xin-Bao Sun, Qing-Yun Chong, Arindam Banerjee, Min Zhang, Zheng-Sheng Wu, Tao Zhu, Vijay Pandey, Peter E Lobie

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
2.1field-weighted citation impact, top 10% 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

3 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Integration of CD34Journal of translational medicine · 2022
    Article
  3. 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

9 authors at 7 institutions in 3 countries.

Qiu-Shi ZhuangCancer Science Institute of Singapore and Department of Pharmacology, National University of Singapore, Singapore, Singapore.
Xin-Bao SunDepartment of Oncology of the First Affiliated Hospital, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
Qing-Yun ChongCancer Science Institute of Singapore and Department of Pharmacology, National University of Singapore, Singapore, Singapore.
Arindam BanerjeeCancer Science Institute of Singapore and Department of Pharmacology, National University of Singapore, Singapore, Singapore.
Min ZhangDepartment of Oncology of the First Affiliated Hospital, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
Zheng-Sheng WuDepartment of Pathology, Anhui Medical University, Hefei, China.
Tao ZhuDepartment of Oncology of the First Affiliated Hospital, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
Vijay PandeyTsinghua Berkeley Shenzhen Institute, Tsinghua Shenzhen International Graduate School, Tsinghua University, Shenzhen, China.
Peter E LobieCancer Science Institute of Singapore and Department of Pharmacology, National University of Singapore, Singapore, Singapore.
Hefei National Center for Physical Sciences at Nanoscale · CNTsinghua–Berkeley Shenzhen Institute · CNAnhui Medical University · CNIndian Institute of Technology Kharagpur · INNational University Cancer Institute, Singapore · SGTsinghua University · CNUniversity of Science and Technology of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

ARTEMIN (ARTN), one of the glial-cell derived neurotrophic factor family of ligands, has been reported to be associated with a number of human malignancies. In this study, the enhanced expression of ARTN in colorectal carcinoma (CRC) was observed; the expression of ARTN positively correlated with lymph node metastases and advanced tumor stages and predicted poor prognosis. Forced expression of ARTN in CRC cells enhanced oncogenic behavior, mesenchymal phenotype, stem cell-like properties and tumor growth and metastasis in a xenograft model. These functions were conversely inhibited by depletion of endogenous ARTN. Forced expression of ARTN reduced the sensitivity of CRC cells to 5-FU treatment; and 5-FU resistant CRC cells harbored enhanced expression of ARTN. The oncogenic functions of ARTN were demonstrated to be mediated by p44/42 MAP kinase dependent expression of CDH2 (CADHERIN 2, also known as N-CADHERIN). Inhibition of p44/42 MAP kinase activity or siRNA mediated depletion of endogenous CDH2 reduced the enhanced oncogenicity and chemoresistance consequent to forced expression of ARTN induced cell functions; and forced expression of CDH2 rescued the reduced mesenchymal properties and resistance to 5-FU after ARTN depletion. In conclusion, ARTN may be of prognostic and theranostic utility in CRC.

Indexed as

ARTEMINCDH2chemoresistancecolorectal carcinomametastasisP44/42 MAPK

Identifiers

PMID34422665
PMCPMC8377398
OpenAlexW3192129808

What OpenQuestion holds

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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.