Evidence map›Paper›PMID 33797657›Full record

ArticleCell biology and toxicology2022

Stanniocalcin-2 promotes cell EMT and glycolysis via activating ITGB2/FAK/SOX6 signaling pathway in nasopharyngeal carcinoma.

Jingquan Li, Zihao Zhang, Xu Feng, Zhuqing Shen, Ji Sun, Xiuwen Zhang, Fengjiao Bu, Midie Xu, Cong Tan, Ziliang Wang

Open access · hybridAbstract read
In one paragraph

Article in Cell biology and toxicology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 8% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

  1. Pooled it
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  11. Stanniocalcin 2 (STC2): a universal tumour biomarker and a potential therapeutical target.Journal of experimental & clinical cancer research : CR · 2022
    Review
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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

10 authors at 4 institutions in 1 country.

Jingquan Li *Center for Single-Cell Omics, School of Public Health, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Zihao Zhang *School of Pharmacy, Anhui Medical University, 81 Meishan Road, Hefei, 230032, Anhui, China.
Xu Feng *Department of Pathology and Tissue Bank, Fudan University Shanghai Cancer Center, 270 Dong'an Road, Shanghai, 200032, China.
Zhuqing ShenDepartment of Pharmacy, Eye & ENT Hospital, Fudan University, Shanghai, 200031, China.
Ji SunDepartment of Pharmacy, Eye & ENT Hospital, Fudan University, Shanghai, 200031, China.
Xiuwen ZhangDepartment of Pharmacy, Eye & ENT Hospital, Fudan University, Shanghai, 200031, China.
Fengjiao BuDepartment of Pharmacy, Eye & ENT Hospital, Fudan University, Shanghai, 200031, China.
Midie XuDepartment of Pathology and Tissue Bank, Fudan University Shanghai Cancer Center, 270 Dong'an Road, Shanghai, 200032, China. xumd27202003@sina.com.
Cong TanDepartment of Pathology and Tissue Bank, Fudan University Shanghai Cancer Center, 270 Dong'an Road, Shanghai, 200032, China. saratancong@yeah.net.
Ziliang WangCenter for Single-Cell Omics, School of Public Health, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China. huf_zlwang@126.com.ORCID 0000-0002-2702-5887
Eye & ENT Hospital of Fudan University · CNFudan University Shanghai Cancer Center · CNShanghai Jiao Tong University · CNAnhui Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Stanniocalcin-2 (STC2) has been proved to regulate a variety of signaling pathways including cell growth, metastasis, and therapeutic resistance. However, the role of STC2 in the regulation of nasopharyngeal carcinoma (NPC) remains poorly understood. In this study, we investigated the regulatory function of STC2 on epithelial-mesenchymal transition (EMT) and glycolysis traits in NPC and revealed the underlying molecular mechanisms. We found that STC2 was highly expressed in primary nasopharyngeal carcinoma tissues and lymph node metastatic tissues. Silencing of STC2 inhibited cell proliferation, invasion, and glycolysis. Further analyses for the clinical samples demonstrated that STC2 expression was associated with the poor clinical progression. Moreover, we demonstrated the interaction of ITGB2 with STC2 and its involvement in STC2-mediated ITGB2/FAK/SOX6 axis. Collectively, our results provide new insights into understanding the regulatory mechanism of STC2 and suggest that the STC2/ITGB2/FAK/SOX6 signaling axis may be a potential therapeutic target for NPC.

Indexed as

Epithelial-Mesenchymal TransitionNasopharyngeal NeoplasmsCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticGlycolysisGlycoproteinsHumansIntercellular Signaling Peptides and ProteinsNasopharyngeal CarcinomaSignal TransductionSOXD Transcription FactorsGlycoproteinsIntercellular Signaling Peptides and ProteinsSOX6 protein, humanSOXD Transcription FactorsteleocalcinEMTGlycolysisNasopharyngeal carcinomaSTC2

Identifiers

PMID33797657
PMCPMC8986754
OpenAlexW3141897560

What OpenQuestion holds

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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.