Evidence map›Paper›PMID 27340870›Full record

ArticleOncotarget2016

ST6Gal-I modulates docetaxel sensitivity in human hepatocarcinoma cells via the p38 MAPK/caspase pathway.

Xixi Chen, Liping Wang, Yujie Zhao, Shiqi Yuan, Qiang Wu, Xiaoling Zhu, Bachir Niang, Shujing Wang, Jianing Zhang

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 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

28 citing papers in PubMed, 46 citations in OpenAlex.

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  8. ST6Gal1: Oncogenic signaling pathways and targets.Frontiers in molecular biosciences · 2022
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  16. The glycosyltransferase ST6Gal-I is enriched in cancer stem-like cells in colorectal carcinoma and contributes to their chemo-resistance.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2018
    Article
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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 3 institutions in 1 country.

Xixi ChenSchool of Life Science and Medicine, Dalian University of Technology, Panjin 124221, Liaoning, China.
Liping WangDepartment of Biochemistry and Molecular Biology, Institute of Glycobiology, Dalian Medical University, Dalian 116044, Liaoning, China.
Yujie ZhaoDepartment of Biochemistry and Molecular Biology, Institute of Glycobiology, Dalian Medical University, Dalian 116044, Liaoning, China.
Shiqi YuanDepartment of Biochemistry and Molecular Biology, Institute of Glycobiology, Dalian Medical University, Dalian 116044, Liaoning, China.
Qiang WuDepartment of Biochemistry and Molecular Biology, Institute of Glycobiology, Dalian Medical University, Dalian 116044, Liaoning, China.
Xiaoling ZhuDepartment of Biochemistry and Molecular Biology, Institute of Glycobiology, Dalian Medical University, Dalian 116044, Liaoning, China.
Bachir NiangDepartment of Biochemistry and Molecular Biology, Institute of Glycobiology, Dalian Medical University, Dalian 116044, Liaoning, China.
Shujing WangDepartment of Biochemistry and Molecular Biology, Institute of Glycobiology, Dalian Medical University, Dalian 116044, Liaoning, China.
Jianing ZhangSchool of Life Science and Medicine, Dalian University of Technology, Panjin 124221, Liaoning, China.
Dalian Medical University · CNDalian University · CNDalian University of Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The β-galactoside α2-6-sialyltransferase 1 (ST6Gal-I) is the principal sialyltransferase responsible for the addition of α2-6-sialic acid to the termini N-glycans on cell surface. Although ST6Gal-I in cancer cell resistance to chemotherapeutics agents has been previously reported, the role of ST6Gal-I in clinical drug resistance of hepatocellular carcinoma (HCC) is not fully understood. In this study, we found that knockdown of ST6Gal-I increased the sensitivity of hepatocarcinoma MHCC97-H cells to docetaxel treatment by instigating the process of apoptosis. Silencing ST6Gal-I expression decreased the survival rate of MHCC97-H cells after docetaxel treatment. Importantly, ST6Gal-I silencing resulted in an increasing of phospho-p38, Bax, Bad, cytochrome c and the cleaved caspase-9, 3 and PARP, while a decreasing of the anti-apoptotic protein Bcl-2. In addition, we found that p38 MAPK and caspase-3 inhibitors can reduce the enhanced apoptosis levels of MHCC97-H cells resulted by either ST6Gal-I silencing or docetaxel treatment. Conversely, exogenous expression of ST6Gal-I in hepatocarcinoma Huh7 cells inhibited apoptotic cell death and prevented docetaxel-induced apoptosis by inhibiting p38 MAPK mediated mitochondrial-dependent pathway. Taken together, these results indicate that ST6Gal-I might play a positive role in mediating the survival of human hepatocarcinoma cells and could be a potential target for gene and antitumor drugs therapy.

Indexed as

Antigens, CDAntineoplastic AgentsApoptosisbeta-D-Galactoside alpha 2-6-SialyltransferaseCarcinoma, HepatocellularCaspasesCell Line, TumorDocetaxelDrug Resistance, NeoplasmHumansLiver NeoplasmsMAP Kinase Signaling Systemp38 Mitogen-Activated Protein KinasesSialyltransferasesTaxoidsAntigens, CDAntineoplastic Agentsbeta-D-Galactoside alpha 2-6-SialyltransferaseCaspasesDocetaxelp38 Mitogen-Activated Protein KinasesSialyltransferasesST6GAL1 protein, humanTaxoidsapoptosisdocetaxelHCCp38 MAPKST6Gal-I

Identifiers

PMID27340870
PMCPMC5239527
OpenAlexW2472409041

What OpenQuestion holds

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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.