Evidence map›Paper›PMID 26318312›Full record

ArticleMolecular and cellular biochemistry2015

MAPK/ERK signaling pathway-induced hyper-O-GlcNAcylation enhances cancer malignancy.

Xinling Zhang, Leina Ma, Jieqiong Qi, Hui Shan, Wengong Yu, Yuchao Gu

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular and cellular biochemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.6field-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

29 citing papers in PubMed, 53 citations in OpenAlex.

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  7. Stress Granules in Cancer.Reviews of physiology, biochemistry and pharmacology · 2023
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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

6 authors at 1 institution in 1 country.

Xinling ZhangKey Laboratory of Marine Drugs, Chinese Ministry of Education; Key Laboratory of Glycoscience & Glycotechnology of Shandong Province; School of Medicine and Pharmacy, Ocean University of China, 5 Yushan Road, Qingdao, 266003, China.
Leina MaKey Laboratory of Marine Drugs, Chinese Ministry of Education; Key Laboratory of Glycoscience & Glycotechnology of Shandong Province; School of Medicine and Pharmacy, Ocean University of China, 5 Yushan Road, Qingdao, 266003, China.
Jieqiong QiKey Laboratory of Marine Drugs, Chinese Ministry of Education; Key Laboratory of Glycoscience & Glycotechnology of Shandong Province; School of Medicine and Pharmacy, Ocean University of China, 5 Yushan Road, Qingdao, 266003, China.
Hui ShanKey Laboratory of Marine Drugs, Chinese Ministry of Education; Key Laboratory of Glycoscience & Glycotechnology of Shandong Province; School of Medicine and Pharmacy, Ocean University of China, 5 Yushan Road, Qingdao, 266003, China.
Wengong YuKey Laboratory of Marine Drugs, Chinese Ministry of Education; Key Laboratory of Glycoscience & Glycotechnology of Shandong Province; School of Medicine and Pharmacy, Ocean University of China, 5 Yushan Road, Qingdao, 266003, China.
Yuchao GuKey Laboratory of Marine Drugs, Chinese Ministry of Education; Key Laboratory of Glycoscience & Glycotechnology of Shandong Province; School of Medicine and Pharmacy, Ocean University of China, 5 Yushan Road, Qingdao, 266003, China. guych@126.com.
Ocean University of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dysregulated MAPK/ERK signaling is implicated in one-third of human tumors and represents an attractive target for the development of anticancer drugs. Similarly, elevated protein O-GlcNAcylation and O-GlcNAc transferase (OGT) are detected in various cancers and serve as attractive novel cancer-specific therapeutic targets. However, the potential connection between them remains unexplored. Here, a positive correlation was found between the activated MAPK/ERK signaling and hyper-O-GlcNAcylation in various cancer types and inhibition of the MAPK/ERK signaling by 10 µM U0126 significantly decreased the expression of OGT and O-GlcNAcylation in H1299, BPH-1 and DU145 cells; then, the pathway analysis of the potential regulators of OGT obtained from the UCSC Genome Browser was done, and ten downstream targets of ERK pathway were uncovered; the following results showed that ELK1, one of the ten targets of ERK pathway, mediated ERK signaling-induced OGT upregulation; finally, the MTT assay and the soft agar assay showed that the inhibition of MAPK/ERK signaling reduced the promotion effect of hyper-O-GlcNAcylation on cancer cell proliferation and anchorage-independent growth. Taken together, our data originally provided evidence for the regulatory mechanism of hyper-O-GlcNAcylation in tumors, which will be helpful for the development of anticancer drugs targeting to hyper-O-GlcNAcylation. This study also provided a new mechanism by which MAPK/ERK signaling-enhanced cancer malignancy. Altogether, the recently discovered oncogenic factor O-GlcNAc was linked to the classical MAPK/ERK signaling which is essential for the maintenance of malignant phenotype of cancers.

Indexed as

MAP Kinase Signaling SystemProtein Processing, Post-TranslationalAntineoplastic AgentsButadienesCell Line, TumorCell ProliferationEnzyme Activationets-Domain Protein Elk-1Extracellular Signal-Regulated MAP KinasesGlycosylationHumansN-AcetylglucosaminyltransferasesNeoplasmsNitrilesProtein Kinase InhibitorsRNA InterferenceAntineoplastic AgentsButadienesELK1 protein, humanets-Domain Protein Elk-1Extracellular Signal-Regulated MAP KinasesN-AcetylglucosaminyltransferasesNitrilesO-GlcNAc transferaseProtein Kinase InhibitorsU 0126CancerMAPK/ERKO-GlcNAcylationOGTPathway Analysis

Identifiers

PMID26318312
OpenAlexW1956798807

What OpenQuestion holds

Textmetadata
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.