Evidence map›Paper›PMID 30484950›Full record

ArticleJournal of cellular and molecular medicine2019

O-GlcNAcylation promotes colorectal cancer progression by regulating protein stability and potential catcinogenic function of DDX5.

Nan Wu, Mingzuo Jiang, Yuying Han, Haiming Liu, Yi Chu, Hao Liu, Jiayi Cao, Qiuqiu Hou, Yu Zhao, Bing Xu and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

30 citing papers in PubMed, 54 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

11 authors at 5 institutions in 1 country.

Nan WuLaboratory of Tissue Engineering, Faculty of Life Science, Northwest University, Xi'an, Shaanxi, China.
Mingzuo JiangState Key Laboratory of Cancer Biology, National Clinical Research Center for Digestive Diseases and Xijing Hospital of Digestive Diseases, Air Force Medical University (Fourth Military Medical University), Xi'an, Shaanxi, China.
Yuying HanLaboratory of Tissue Engineering, Faculty of Life Science, Northwest University, Xi'an, Shaanxi, China.
Haiming LiuCollege of Computer Science and Technology, Jilin University, Changchun, Jilin, China.
Yi ChuState Key Laboratory of Cancer Biology, National Clinical Research Center for Digestive Diseases and Xijing Hospital of Digestive Diseases, Air Force Medical University (Fourth Military Medical University), Xi'an, Shaanxi, China.
Hao LiuState Key Laboratory of Cancer Biology, National Clinical Research Center for Digestive Diseases and Xijing Hospital of Digestive Diseases, Air Force Medical University (Fourth Military Medical University), Xi'an, Shaanxi, China.
Jiayi CaoLaboratory of Tissue Engineering, Faculty of Life Science, Northwest University, Xi'an, Shaanxi, China.
Qiuqiu HouLaboratory of Tissue Engineering, Faculty of Life Science, Northwest University, Xi'an, Shaanxi, China.
Yu ZhaoLaboratory of Tissue Engineering, Faculty of Life Science, Northwest University, Xi'an, Shaanxi, China.
Bing XuDepartment of Gastroenterology, Second Affiliated Hospital of Xi'an Jiao tong University, Xi'an, Shaanxi, China.
Xin XieLaboratory of Tissue Engineering, Faculty of Life Science, Northwest University, Xi'an, Shaanxi, China.
Northwest University · CNAir Force Medical University · CNJilin University · CNSecond Affiliated Hospital of Xi'an Jiaotong University · CNXijing Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The RNA helicase p68 (DDX5), a key player in RNA metabolism, belongs to the DEAD box family and is involved in the development of colorectal cancer. Here, we found both DDX5 and O-GlcNAcylation are up-regulated in colorectal cancer. In addition, DDX5 protein level is significantly positively correlated with the expression of O-GlcNAcylation. Although it was known DDX5 protein could be regulated by post-translational modification (PTM), how O-GlcNAcylation modification regulated of DDX5 remains unclear. Here we show that DDX5 interacts directly with OGT in the SW480 cell line, which is the only known enzyme that catalyses O-GlcNAcylation in humans. Meanwhile, O-GlcNAcylation could promote DDX5 protein stability. The OGT-DDX5 axis affects colorectal cancer progression mainly by regulating activation of the AKT/mTOR signalling pathway. Taken together, these results indicated that OGT-mediated O-GlcNAcylation stabilizes DDX5, promoting activation of the AKT/mTOR signalling pathway, thus accelerating colorectal cancer progression. This study not only reveals the novel functional of O-GlcNAcylation in regulating DDX5, but also reveals the carcinogenic effect of the OGT-DDX5 axis in colorectal cancer.

Indexed as

Protein Processing, Post-TranslationalAnimalsApoptosisBiomarkers, TumorCell MovementCell ProliferationColorectal NeoplasmsDEAD-box RNA HelicasesDisease ProgressionGene Expression Regulation, NeoplasticGlycosylationHumansMaleMiceMice, Inbred BALB CMice, NudeAKT1 protein, humanBiomarkers, TumorDdx5 protein, humanDEAD-box RNA HelicasesMTOR protein, humanN-AcetylglucosaminyltransferasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesAKTColorectal cancerDDX5mTORO-GlcNAcylation

Identifiers

PMID30484950
PMCPMC6349181
OpenAlexW2903299497

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.