Evidence map›Paper›PMID 30151927›Full record

ArticleCancer science2018

Inhibin B suppresses anoikis resistance and migration through the transforming growth factor-β signaling pathway in nasopharyngeal carcinoma.

Guoying Zou, Biqiong Ren, Yi Liu, Yin Fu, Pan Chen, Xiayu Li, Shudi Luo, Junyu He, Ge Gao, Zhaoyang Zeng and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

32 citing papers in PubMed, 42 citations in OpenAlex.

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  17. Evolving roles of activins and inhibins in ovarian cancer pathophysiology.American journal of physiology. Cell physiology · 2023
    Review
  18. Lrriq1 is an essential factor for fertility by suppressing apoptosis.Journal of assisted reproduction and genetics · 2022
    Article
  19. Article
  20. RNA mFrontiers in immunology · 2022
    Article
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

15 authors at 3 institutions in 1 country.

Guoying ZouDepartment of Medical Laboratory Science, Xiangya School of Medicine, Central South University, Changsha, China.ORCID http://orcid.org/0000-0003-0719-9975
Biqiong RenDepartment of Clinical Laboratory, Brain Hospital of Hunan Province, Changsha, China.
Yi LiuDepartment of Medical Laboratory Science, Xiangya School of Medicine, Central South University, Changsha, China.
Yin FuDepartment of Medical Laboratory, Hunan University of Traditional Chinese Medicine, Changsha, China.
Pan ChenHunan Cancer Hospital and The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, China.
Xiayu LiHunan Cancer Hospital and The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, China.
Shudi LuoDepartment of Medical Laboratory, Hunan University of Traditional Chinese Medicine, Changsha, China.
Junyu HeDepartment of Clinical Laboratory, Brain Hospital of Hunan Province, Changsha, China.
Ge GaoDepartment of Medical Laboratory Science, Xiangya School of Medicine, Central South University, Changsha, China.
Zhaoyang ZengHunan Cancer Hospital and The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, China.
Wei XiongHunan Cancer Hospital and The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, China.ORCID http://orcid.org/0000-0003-1635-8173
Guiyuan LiThe Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Cancer Research Institute, Central South University, Changsha, China.
Yumei HuangHunan Cancer Hospital and The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, China.
Keqian XuDepartment of Medical Laboratory Science, Xiangya School of Medicine, Central South University, Changsha, China.
Wenling ZhangDepartment of Medical Laboratory Science, Xiangya School of Medicine, Central South University, Changsha, China.
Central South University · CNHunan University of Traditional Chinese Medicine · CNSecond People Hospital of Hunan · CN

Funding

National Natural Science Foundation of China 81101509National Natural Science Foundation of China 81402307National Natural Science Foundation of China 81672688
6 · The paper itself

Abstract

Inhibin B (INHBB), a heterodimer of a common α-subunit and a βB-subunit, is a glycoprotein belonging to the transforming growth factor-β (TGF-β) family. In this study, we observed INHBB expression was reduced in nasopharyngeal carcinoma (NPC) tissues compared to non-tumor nasopharyngeal epithelium tissues, and INHBB was associated with lymph node metastasis, stage of disease, and clinical progress. Positive expression of INHBB in NPC predicted a better prognosis (overall survival, P = 0.038). However, the molecular mechanisms of INHBB have not been addressed in NPC. We induced anoikis-resistant cells in NPC cell lines under anchorage-independent conditions, then found epithelial-mesenchymal transition markers changed, cell apoptosis decreased, cell cycle was modified, and invasion strengthened in anoikis-resistant NPC cells. These anoikis-resistant NPC cells showed decreased expression of INHBB compared with adhesion cells. Furthermore, INHBB was found to influence the above-mentioned changes. In the anoikis-resistant NPC cells with INHBB overexpression, apoptotic cells increased, S phase cells weakened, vimentin, matrix metallopeptidase-9, and vascular endothelial growth factor A expression were downregulated, and E-cadherin expression was upregulated, and vice versa in knockdown of INHBB (INHBB shRNA) anoikis-resistant NPC cells. Diminished INHBB expression could activate the TGF-β pathway to phosphorylate Smad2/3 and form complexes in the nucleus, which resulted in the above changes. Thus, our results revealed for the first time that INHBB could suppress anoikis resistance and migration of NPC cells by the TGF-β signaling pathway, decrease p53 overexpression, and could serve as a potential biomarker for NPC metastasis and prognosis as well as a therapeutic application.

Indexed as

Down-RegulationAdolescentAdultAgedAnoikisCarcinomaCell Line, TumorCell MovementEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansInhibin-beta SubunitsMaleMiddle AgedNasopharyngeal CarcinomaINHBB protein, humanInhibin-beta SubunitsTP53 protein, humanTransforming Growth Factor betaTumor Suppressor Protein p53anoikisinhibin Bmetastasisnasopharyngeal carcinomaTGF-β

Identifiers

PMID30151927
PMCPMC6215878
OpenAlexW2888945647

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.