Evidence map›Paper›PMID 35513377›Full record

ArticleCell death discovery2022

FAM126A interacted with ENO1 mediates proliferation and metastasis in pancreatic cancer via PI3K/AKT signaling pathway.

Yongning Li, Ying Li, Jun Luo, Xueqin Fu, Peng Liu, Songbai Liu, Yaozhen Pan

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2022. 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
2.1field-weighted citation impact, top 12% 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, 26 citations in OpenAlex.

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  19. Role of ENO1 and its targeted therapy in tumors.Journal of translational medicine · 2024
    Review
  20. The regulatory roles and clinical significance of glycolysis in tumor.Cancer communications (London, England) · 2024
    Review
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

7 authors at 2 institutions in 1 country.

Yongning Li *College of Clinical Medicine, Guizhou Medical University, Guiyang, Guizhou, China.ORCID http://orcid.org/0000-0003-0912-4694
Ying Li *College of Clinical Medicine, Guizhou Medical University, Guiyang, Guizhou, China.
Jun Luo *College of Clinical Medicine, Guizhou Medical University, Guiyang, Guizhou, China.
Xueqin FuDepartment of Breast Surgery, Guizhou Provincial People's Hospital, Guiyang, Guizhou, China.
Peng LiuCollege of Clinical Medicine, Guizhou Medical University, Guiyang, Guizhou, China.
Songbai LiuCollege of Clinical Medicine, Guizhou Medical University, Guiyang, Guizhou, China.
Yaozhen PanCollege of Clinical Medicine, Guizhou Medical University, Guiyang, Guizhou, China. panyaozhen@gmc.edu.cn.ORCID http://orcid.org/0000-0002-9300-382X
Guiyang Medical University · CNGuizhou Provincial People's Hospital · CN

Funding

Guizhou Science and Technology Department (Department of Science and Technology, Guizhou Province) grant number Qiankehe Project-QKH[2021] General 100
6 · The paper itself

Abstract

Pancreatic cancer (PC) is a common digestive system carcinoma with high mortality rate mostly due to aberrant growth and distant metastasis. Current researches demonstrated that Family Sequence Similarities (FAMs) have been involving in tumor development, and which subfamily has the function of promoting or inhibiting tumors and its in-depth molecular mechanism remains unclear. Based on the Gene Expression Omnibus (GEO), the Gene Expression Profiling Interactive Analysis (GEPIA2), we observed that FAM126A is in high expressed level among PC tissues and contributes to worse progression of PC, which was validated by PC tissue microarray. Function assay indicated that overexpression of FAM126A accelerates PC cell proliferation, invasion and migration in vitro, as well as liver cancer metastasis in vivo. Further, we found that FAM126A induces epithelial-mesenchymal transition (EMT), including the downregulation of E-cadherin epithelial marker expression, and the upregulation of N-cadherin, Vimentin, and Snail, mesenchymal marker expression. By co-localization and co-immunoprecipitation assays, we confirmed that FAM126A directly interacts with ENO1, which was a key activator of the PI3K/AKT signaling pathway. Furthermore, ENO1 knockdown reversed cell proliferation, migration, and invasion of PC cells promoted by FAM126A overexpression in vitro and in vivo. In general, these results verified FAM126A is an oncogene interacting with ENO1 in PC by activating PI3K/AKT signaling pathway.

Identifiers

PMID35513377
PMCPMC9072533
OpenAlexW4228998511

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.