Evidence map›Paper›PMID 31789389›Full record

ArticleInternational journal of oncology2020

UNC5C‑knockdown enhances the growth and metastasis of breast cancer cells by potentiating the integrin α6/β4 signaling pathway.

Mingjing Yuan, Fuan Xie, Xianyuan Xia, Kai Zhong, Lanlan Lian, Shihui Zhang, Li Yuan, Jun Ye

Open access · hybridAbstract read
In one paragraph

Article in International journal of oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.4field-weighted citation impact, top 42% 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

12 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
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  7. Research progress of the netrins and their receptors in cancer.Journal of cellular and molecular medicine · 2024
    Review
  8. Genes · 2024
    Article
  9. Article
  10. 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

8 authors at 2 institutions in 1 country.

Mingjing YuanState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, Fujian 361102, P.R. China.
Fuan XieState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, Fujian 361102, P.R. China.
Xianyuan XiaState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, Fujian 361102, P.R. China.
Kai ZhongState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, Fujian 361102, P.R. China.
Lanlan LianDepartment of Laboratory Medicine, Xiang'an Hospital of Xiamen University, Xiamen University, Xiamen, Fujian 361102, P.R. China.
Shihui ZhangSchool of Life Science, Central South University, Changsha, Hunan 410083, P.R. China.
Li YuanState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, Fujian 361102, P.R. China.
Jun YeState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, Fujian 361102, P.R. China.
Xiamen University · CNCentral South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Unc‑5 Netrin Receptor C (UNC5C) is a netrin‑1 dependence receptor that mediates the induction of apoptosis in the absence of netrin‑1. The present study found that UNC5C is heterogeneously expressed in breast cancer cell lines. By knocking down UNC5C in SK‑BR‑3 and ZR‑75‑30 cells and overexpressing UNC5c in MDA‑MB‑231 cells, it was demonstrated that UNC5C exerts an inhibitory effect on the growth and metastasis of breast cancer cells. The mechanism involved a UNC5C‑knockdown‑induced enhancement of matrix metalloproteinase (MMP)3, MMP7, MMP9 and MMP10 expression via activation of the PI3K/AKT, ERK and p38 MAPK signaling pathways. Notably, UNC5C directly interacted with integrin α6, which is involved in the growth and metastasis of breast cancer cells. Additionally, UNC5C‑knockdown enhanced the phosphorylation of FAK and SRC, which are key kinases in the netrin‑1/Unc5C and netrin‑1/integrin α6/β4 signaling pathways. This suggests that netrin‑1 functions as an integrator for both the netrin‑1/Unc5C and netrin‑1/integrin α6/β4 signaling pathways. UNC5C‑knockdown potentiated netrin‑1/integrin α6/β4 signaling. Given that UNC5C‑knockdown inhibited integrin‑liked protein kinase phosphorylation at Thr‑173, at least in SK‑BR‑3 cells, this may be an inhibitory phosphorylation site rather than activating phosphorylation site for relaying integrin signaling.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsApoptosisBiomarkers, TumorBreast NeoplasmsCell ProliferationFemaleHumansIntegrin alpha6Integrin beta4Lung NeoplasmsMiceMice, Inbred BALB CMice, NudeNetrin ReceptorsSignal TransductionBiomarkers, TumorIntegrin alpha6Integrin beta4ITGA6 protein, humanITGB4 protein, humanNetrin ReceptorsUNC5C protein, human

Identifiers

PMID31789389
PMCPMC6910211
OpenAlexW2992588420

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.