Evidence map›Paper›PMID 27588482›Full record

ArticleOncotarget2016

ST6Gal-I overexpression facilitates prostate cancer progression via the PI3K/Akt/GSK-3β/β-catenin signaling pathway.

Anwen Wei, Bo Fan, Yujie Zhao, Han Zhang, Liping Wang, Xiao Yu, Qingmin Yuan, Deyong Yang, Shujing Wang

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 6% 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

51 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.

  1. Pooled it
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  6. Expression of 9-Life (Basel, Switzerland) · 2025
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  10. Glycosylation in Cancer.Handbook of experimental pharmacology · 2025
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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

9 authors at 1 institution in 1 country.

Anwen WeiDepartment of Biochemistry and Molecular Biology, Institute of Glycobiology, Dalian Medical University, Dalian, 116044, Liaoning Province, China.
Bo FanDepartment of Urology, First Affiliated Hospital of Dalian Medical University, Dalian, 116011, Liaoning Province, China.
Yujie ZhaoDepartment of Biochemistry and Molecular Biology, Institute of Glycobiology, Dalian Medical University, Dalian, 116044, Liaoning Province, China.
Han ZhangDepartment of Biochemistry and Molecular Biology, Institute of Glycobiology, Dalian Medical University, Dalian, 116044, Liaoning Province, China.
Liping WangDepartment of Biochemistry and Molecular Biology, Institute of Glycobiology, Dalian Medical University, Dalian, 116044, Liaoning Province, China.
Xiao YuDepartment of Pathology, Dalian Medical University, Dalian, 116044, Liaoning Province, China.
Qingmin YuanDepartment of Biochemistry and Molecular Biology, Institute of Glycobiology, Dalian Medical University, Dalian, 116044, Liaoning Province, China.
Deyong YangDepartment of Urology, First Affiliated Hospital of Dalian Medical University, Dalian, 116011, Liaoning Province, China.
Shujing WangDepartment of Biochemistry and Molecular Biology, Institute of Glycobiology, Dalian Medical University, Dalian, 116044, Liaoning Province, China.
Dalian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

ST6Gal-I sialyltransferase adds α2,6-linked sialic acids to the terminal ends of glycan chains of glycoproteins and glycolipids. ST6Gal-I is reportedly upregulated in many cancers, including hepatocellular carcinoma, ovarian cancer and breast cancer. However, the expression and function of ST6Gal-I in prostate cancer (PCa) and the mechanism underlying this function remain largely unknown. In this study, we observed that ST6Gal-I expression was upregulated in human PCa tissues compared to non-malignant prostate tissues. High ST6Gal-I expression was positively correlated with Gleason scores, seminal vesicle involvement and poor survival in patients with PCa. ST6Gal-I knockdown in aggressive prostate cancer PC-3 and DU145 cells significantly inhibited the proliferation, growth, migration and invasion capabilities of these cells. ST6Gal-I knockdown decreased the levels of several PI3K/Akt/GSK-3β/ β-catenin pathway components, such as p-PI3K, (Ser473)p-Akt, (Ser9)p-GSK-3β and β-catenin. Furthermore, targeting this pathway with a PI3K inhibitor or Akt RNA interference decreased p-Akt, p-GSK-3β and β-catenin expression, resulting in decreased PC-3 and DU145 proliferation, migration and invasion. Taken together, these results indicate that ST6Gal-I plays a critical role in cell proliferation and invasion via the PI3K/Akt/GSK-3β/β-catenin signaling pathway during PCa progression and that it might be a promising target for PCa prognosis determination and therapy.

Indexed as

AgedAntigens, CDbeta Cateninbeta-D-Galactoside alpha 2-6-SialyltransferaseCarcinogenesisCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticGlycogen Synthase Kinase 3 betaHumansMaleOncogene Protein v-aktPhosphatidylinositol 3-KinasesProstatic NeoplasmsRNA, Small InterferingAntigens, CDbeta Cateninbeta-D-Galactoside alpha 2-6-SialyltransferaseGlycogen Synthase Kinase 3 betaOncogene Protein v-aktPhosphatidylinositol 3-KinasesRNA, Small InterferingSialyltransferasesST6GAL1 protein, human6-sialic acidprognosisproliferation and invasionprostate cancerST6Gal-Iα2

Identifiers

PMID27588482
PMCPMC5323162
OpenAlexW2509135444

What Socratic 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 Socratic graph.