Evidence map›Paper›PMID 35860571›Full record

ArticleFrontiers in oncology2022

PDIA2 Bridges Endoplasmic Reticulum Stress and Metabolic Reprogramming During Malignant Transformation of Chronic Colitis.

Jie Tao, Lin Yin, Ao Wu, Jiaoli Zhang, Jingpu Zhang, Huichun Shi, Siyuan Liu, Liangfei Niu, Li Xu, Yanling Feng and 7 more

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

Article in Frontiers in oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

13 citing papers in PubMed, 17 citations in OpenAlex.

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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

17 authors at 2 institutions in 1 country.

Jie TaoScientific Research Institute, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China.
Lin YinScientific Research Institute, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China.
Ao WuScientific Research Institute, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China.
Jiaoli ZhangScientific Research Institute, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China.
Jingpu ZhangScientific Research Institute, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China.
Huichun ShiScientific Research Institute, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China.
Siyuan LiuThe College of Information, Mechanical and Electrical Engineering, Shanghai Normal University, Shanghai, China.
Liangfei NiuScientific Research Institute, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China.
Li XuScientific Research Institute, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China.
Yanling FengClinical Pathology Laboratory, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China.
Shixian LianDepartment of Surgery, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China.
Lei LiDepartment of Surgery, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China.
Liyan ZengDepartment of Clinical Research Center, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China.
Xianmin MengDepartment of Clinical Research Center, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China.
Xiaohui ZhouAnimal Research Center, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China.
Tiefu LiuScientific Research Institute, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China.
Lijun ZhangScientific Research Institute, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China.
Shanghai Public Health Clinical Center · CNShanghai Normal University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Chronic inflammation contributes to approximately 20% of cancers; the underlying mechanisms are still elusive. Here, using an animal model of colitis to colon-cancerous transformation, we demonstrated that endoplasmic reticulum (ER) stress couples with metabolic reprogramming to promote a malignant transformation of chronic inflammation. Methods: The animal model for chronic colitis to colon-cancerous transformation was established in C57BL/6N mice by azoxymethane (AOM) and dextran sodium sulfate (DSS) treatments. The differential proteins in control and AOM/DSS-treated colon mucosa were determined using proteomic analysis; the kinetics of metabolic modifications were monitored by mitochondrial oxygen flux, extracellular acidification, and targeted metabolomics; the molecule linker between ER stress and metabolic modifications were identified by coimmunoprecipitation, KEGG pathway analysis, and the subcutaneous tumor model using gene-specific knockdown colon cancer cells. Tissue array analysis were used to evaluate the differential protein in cancer and cancer-adjacent tissues. Results: AOM/DSS treatment induced 38 tumors in 10 mice at the 14th week with the mean tumor size 9.35 ± 3.87 mm Conclusions: Persistent ER stress reprograms the metabolism to promote the malignant transformation of chronic colitis; PDIA2 serves as a molecule linker between ER stress and metabolic reprogramming. The inhibition of ER stress restores metabolic homeostasis and attenuates the cancerous transformation of chronic inflammation.

Indexed as

chronic colitiscolon cancerendoplasmic reticulum stressmalignant transformationmetabolic reprogrammingPDIA2

Identifiers

PMID35860571
PMCPMC9289542
OpenAlexW4283790712

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.