Evidence map›Paper›PMID 27557506›Full record

ArticleOncotarget2016

The requirement of SEPT2 and SEPT7 for migration and invasion in human breast cancer via MEK/ERK activation.

Nianzhu Zhang, Lu Liu, Ning Fan, Qian Zhang, Weijie Wang, Mingnan Zheng, Lingfei Ma, Yan Li, Lei Shi

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

42 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
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  10. Effects of theAnimals : an open access journal from MDPI · 2023
    Article
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  16. Article
  17. Effects ofFrontiers in molecular neuroscience · 2022
    Article
  18. Article
  19. Septins, a cytoskeletal protein family, with emerging role in striated muscle.Journal of muscle research and cell motility · 2021
    Review
  20. Septins in Infections: Focus on Viruses.Pathogens (Basel, Switzerland) · 2021
    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

9 authors at 3 institutions in 1 country.

Nianzhu ZhangInstitute of Cancer Stem Cell, Cancer Center, Dalian Medical University, Dalian, 116044, Liaoning, P.R.China.
Lu LiuCollege of Basic Medical Sciences, Dalian Medical University, Dalian, 116044 Liaoning, P.R.China.
Ning FanCollege of Basic Medical Sciences, Dalian Medical University, Dalian, 116044 Liaoning, P.R.China.
Qian ZhangInstitute of Cancer Stem Cell, Cancer Center, Dalian Medical University, Dalian, 116044, Liaoning, P.R.China.
Weijie WangInstitute of Cancer Stem Cell, Cancer Center, Dalian Medical University, Dalian, 116044, Liaoning, P.R.China.
Mingnan ZhengDepartment of Gynecology and Obstetrics, Dalian Municipal Central Hospital Affiliated to Dalian Medical University, Dalian, 116033, Liaoning, P.R.China.
Lingfei MaThe First Affiliated Hospital of Dalian Medical University, Dalian, 116011, Liaoning, P.R.China.
Yan LiCollege of Basic Medical Sciences, Dalian Medical University, Dalian, 116044 Liaoning, P.R.China.
Lei ShiInstitute of Cancer Stem Cell, Cancer Center, Dalian Medical University, Dalian, 116044, Liaoning, P.R.China.
Dalian Medical University · CNChinese Academy of Sciences · CNDalian Municipal Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Septins are a novel class of GTP-binding cytoskeletal proteins evolutionarily conserved from yeast to mammals and have now been found to play a contributing role in a broad range of tumor types. However, their functional importance in breast cancer remains largely unclear. Here, we demonstrated that pharmaceutical inhibition of global septin dynamics would greatly suppress proliferation, migration and invasiveness in breast cancer cell lines. We then examined the expression and subcellular distribution of the selected septins SEPT2 and SEPT7 in breast cancer cells, revealing a rather variable localization of the two proteins with cell cycle progression. To determine the role of both septins in mediating malignant behavior of cancer cells, we used RNA silencing to specifically deplete endogenous SEPT2 or SEPT7 in highly invasive breast cancer cell line MDA-MB-231. Our findings showed that SEPT2/7 depletion had virtually identical inhibitory effects on cellular proliferation, apoptosis, migration and invasion. Moreover, the opposite performance in migration and invasion was observed after enforced expression of SEPT2/7 in the same cell line. We further demonstrated MEK/ERK activation, but not other MAPKs and AKT, was positively correlated with the protein levels of SEPT2 and SEPT7. Additionally, in SEPT2/7-overexpressing cells, the MEK specific inhibitor U0126 was able to correct the high active status of MEK/ERK while normalizing the increased invasive behaviors of these cells. Taken together, these results strongly suggest that SEPT2 and SEPT7 are involved in breast carcinogenesis and may serve as valuable therapeutic targets for breast cancer.

Indexed as

MAP Kinase Signaling SystemApoptosisBreast NeoplasmsButadienesCarcinogenesisCell CycleCell Cycle ProteinsCell Line, TumorCell MovementCell ProliferationEnzyme InhibitorsFemaleGene Knockdown TechniquesHumansHuman Umbilical Vein Endothelial CellsMAP Kinase Kinase KinasesButadienesCell Cycle ProteinsEnzyme InhibitorsMAP Kinase Kinase KinasesN-(2-chloro-4-pyridyl)-N'-phenylureaNitrilesPhenylurea CompoundsProto-Oncogene Proteins c-aktPyridinesRNA, Small InterferingSEPTIN2 protein, humanSEPTIN7 protein, humanSeptinsU 0126breast cancerforchlorfenuroninvasionMAPKseptin

Identifiers

PMID27557506
PMCPMC5308674
OpenAlexW2510028826

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.