Evidence map›Paper›PMID 33064958›Full record

ArticleCancer biology & therapy2020

FGF13 interaction with SHCBP1 activates AKT-GSK3α/β signaling and promotes the proliferation of A549 cells.

Hongzhao Lu, Meichen Yin, Ling Wang, Jia Cheng, Wei Cheng, Huanping An, Tao Zhang

Open access · bronzeAbstract read
In one paragraph

Article in Cancer biology & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

19 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
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  5. Molecular Mechanism of theAnimals : an open access journal from MDPI · 2025
    Article
  6. SHCBP1 promotes cisplatin resistance of ovarian cancer through AKT/mTOR/Autophagy pathway.Apoptosis : an international journal on programmed cell death · 2025
    Article
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  13. Overexpression ofFrontiers in cell and developmental biology · 2024
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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

7 authors at 2 institutions in 1 country.

Hongzhao LuSchool of Biological Science and Engineering, Shaanxi University of Technology , Hanzhong, Shaanxi, China.
Meichen YinSchool of Biological Science and Engineering, Shaanxi University of Technology , Hanzhong, Shaanxi, China.
Ling WangSchool of Biological Science and Engineering, Shaanxi University of Technology , Hanzhong, Shaanxi, China.
Jia ChengSchool of Biological Science and Engineering, Shaanxi University of Technology , Hanzhong, Shaanxi, China.
Wei ChengDepartment of Cell Biology and Genetics, School of Basic Medical Sciences, Jiaotong University Health Center , Xi'an, Shaanxi, China.
Huanping AnDepartment of Pharmacy and Medical Technology, Hanzhong Vocational and Technical College , Hanzhong, Shaanxi, China.
Tao ZhangSchool of Biological Science and Engineering, Shaanxi University of Technology , Hanzhong, Shaanxi, China.
Shaanxi University of Technology · CNXi'an Jiaotong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

FGF13, a member of the FGF subfamily, has been found to be highly expressed in cancer cells such as prostate cancer, melanoma, glioma and multiple myeloma. However, the mechanism of FGF13 function during cancer cell proliferation remains to be unexplored, especially Non-small cell lung cancer (NSCLC). In this study, the cell proliferation effect of FGF13 on A549 cells was checked by CCK-8, clone formation, Ki67 immunofluorescence staining and Flow Cytometry assay. Localization of FGF13 within A549 cells was performed with confocal laser scanning microscope. The protein variations and interaction were measured by western blotting and co-immunoprecipitation analysis. It showed that FGF13 was mainly distributed in the cytoplasm and exhibited a high expression level in A549 cells. High expression of FGF13 activated AKT-GSK3 signaling pathway, and inhibited the activity of p21 and p27. Thus, FGF13 enhanced the process of transition from G1 to S phase and promoted A549 cells proliferation. Furthermore, the interaction between FGF13 and SHCBP1 was confirmed. Meanwhile, FGF13 and SHCBP1 had a cooperative effect to accelerate the cell cycle progression, especially the ability to promote cell proliferation is significantly enhanced via protein interaction. Hence, we conclude that FGF13 played a positive regulation role during A549 cells proliferation. FGF13 interacted with SHCBP1 to facilitate cell cycle progression, providing new insights into deep understanding of non-small cell lung cancer mechanisms of proliferation and regulation function of FGF13.

Indexed as

A549 CellsCarcinoma, Non-Small-Cell LungCell ProliferationFibroblast Growth FactorsGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHEK293 CellsHumansLung NeoplasmsProto-Oncogene Proteins c-aktShc Signaling Adaptor ProteinsSignal Transductionfibroblast growth factor 13Fibroblast Growth FactorsGlycogen Synthase Kinase 3glycogen synthase kinase 3 alphaGlycogen Synthase Kinase 3 betaGSK3B protein, humanProto-Oncogene Proteins c-aktSHCBP1 protein, humanShc Signaling Adaptor Proteinscell proliferationFGF13Non-small cell lung cancerSHCBP1

Identifiers

PMID33064958
PMCPMC7678946
OpenAlexW3093388481

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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.