Evidence map›Paper›PMID 34719306›Full record

ArticleCell transplantation

MsrB1 Promotes Proliferation and Invasion of Colorectal Cancer Cells via GSK-3β/β-catenin Signaling Axis.

Xiao-Yu Chen, Sheng-Yong Yang, Xiao-Jie Ruan, Hong-Yue Ding, Ning-Xi Wang, Fang Liu, Jia-Chu Li, Yi Li

Open access · goldAbstract read
In one paragraph

Article in Cell transplantation. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

9 citing papers in PubMed, 14 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

8 authors at 3 institutions in 2 countries.

Xiao-Yu ChenDepartment of Biochemistry and Molecular Biology, Molecular Medicine and Cancer Research Center, College of Basic Medicine, Chongqing Medical University, Chongqing, China.
Sheng-Yong YangDepartment of Biochemistry and Molecular Biology, Molecular Medicine and Cancer Research Center, College of Basic Medicine, Chongqing Medical University, Chongqing, China.ORCID 0000-0001-7312-0255
Xiao-Jie RuanDivision of Life Sciences, Department of Biochemical and Biomedical Science, Science Centre, The Chinese University of Hong Kong, Shatin, Hong Kong, China.
Hong-Yue DingDepartment of Biochemistry and Molecular Biology, Molecular Medicine and Cancer Research Center, College of Basic Medicine, Chongqing Medical University, Chongqing, China.
Ning-Xi WangDepartment of Biochemistry and Molecular Biology, Molecular Medicine and Cancer Research Center, College of Basic Medicine, Chongqing Medical University, Chongqing, China.
Fang LiuThe First Clinical College, Chongqing Medical University, Chongqing, China.
Jia-Chu LiDepartment of Oncology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Yi LiDepartment of Biochemistry and Molecular Biology, Molecular Medicine and Cancer Research Center, College of Basic Medicine, Chongqing Medical University, Chongqing, China.
Chongqing Medical University · CNChinese University of Hong Kong · HKThe Affiliated Yongchuan Hospital of Chongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Methionine sulfoxide reductase B1 (MsrB1) can catalyze both free and protein-bound R-methionine sulfoxides (R-MetO) to methionine (Met). It has been reported that MsrB1 plays an important role in the development of HCC and human bone osteosarcoma. However, little is known about the functions of MsrB1 in human colorectal cancer (CRC). Herein, we detected MsrB1 expression level in CRC tissue and cell lines, and investigated the effect of MsrB1 knockdown on CRC phenotypes and possible mechanisms involved in. The results showed that MsrB1 was highly expressed in both CRC tissues and cell lines, and that cell proliferation, migration and invasion were significantly inhibited, but apoptosis was increased after MsrB1 knockdown in colorectal cancer HCT116 and RKO cell lines, compared to control siRNA group. In addition, E-cadherin protein level was increased, vimentin and Snail protein were greatly decreased after knockdown of MsrB1 in cells. Furthermore, pGSK-3β (Ser9) and β-catenin protein levels were reduced, the promoter activity of TCF/LEF construction was inhibited after MsrB1 knockdown in cells, suggesting that GSK-3β/β-catenin signaling axis was involved in the tumorigenesis of CRC. In conclusion, the oncogenic role and related mechanisms of MsrB1 in CRC discovered in our work determined the potential role of MsrB1 as a biomarker and may provide a new target for clinical therapy of CRC.

Indexed as

beta CateninCell ProliferationColorectal NeoplasmsGlycogen Synthase Kinase 3 betaHumansMethionine Sulfoxide ReductasesNeoplasm InvasivenessSignal TransductionTransfectionbeta CateninGlycogen Synthase Kinase 3 betamethionine sulfoxide reductaseMethionine Sulfoxide Reductasescell proliferationcolorectal cancer cellsepithelial-mesenchymal transitionGSK-3β /β-catenin signaling pathwaymethionine sulfoxide reductase B1

Identifiers

PMID34719306
PMCPMC8558597
OpenAlexW3208869020

What OpenQuestion holds

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LicenceCC BY-NC
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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.