Evidence map›Paper›PMID 27729799›Full record

ArticleOncoTargets and therapy2016

The role of semaphorin 4D in tumor development and angiogenesis in human breast cancer.

Hongchao Jiang, Ceshi Chen, Qiangming Sun, Jing Wu, Lijuan Qiu, Change Gao, Weiqing Liu, Jun Yang, Nie Jun, Jian Dong

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

25 citing papers in PubMed, 37 citations in OpenAlex.

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  15. The Role of Semaphorins in Metabolic Disorders.International journal of molecular sciences · 2020
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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

10 authors at 4 institutions in 1 country.

Hongchao JiangDepartment of Oncology, The Affiliated Children's Hospital of Kunming Medical University; Department of Oncology, The Third Affiliated Hospital of Kunming Medical University, Yunnan Provincial Tumor Hospital.
Ceshi ChenKey Laboratory of Animal Models and Human Disease Mechanisms of Chinese Academy of Sciences and Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences.
Qiangming SunMolecular Epidemiology Joint Laboratory, Institute of Medical Biology, Chinese Academy of Medical Sciences, Peking Union Medical College.
Jing WuKey Laboratory of Animal Models and Human Disease Mechanisms of Chinese Academy of Sciences and Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences.
Lijuan QiuMolecular Epidemiology Joint Laboratory, Institute of Medical Biology, Chinese Academy of Medical Sciences, Peking Union Medical College.
Change GaoDepartment of Oncology, The First Affiliated Hospital of Kunming Medical University, Kunming, People's Republic of China.
Weiqing LiuDepartment of Oncology, The First Affiliated Hospital of Kunming Medical University, Kunming, People's Republic of China.
Jun YangDepartment of Oncology, The First Affiliated Hospital of Kunming Medical University, Kunming, People's Republic of China.
Nie JunDepartment of Oncology, The Third Affiliated Hospital of Kunming Medical University, Yunnan Provincial Tumor Hospital.
Jian DongDepartment of Oncology, The Third Affiliated Hospital of Kunming Medical University, Yunnan Provincial Tumor Hospital.
Kunming Medical University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNFirst Affiliated Hospital of Kunming Medical University · CNKunming Institute of Zoology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSemaphorin 4D (Sema4D) is highly expressed in certain types of tumors and functions in the regulation of tumor angiogenesis and growth. However, it is still not clear regarding the roles of Sema4D in breast cancer. This study was designed to explore the effects of Sema4D on proliferation, cell cycle progression, apoptosis, invasion, migration, tumor growth, and angiogenesis in breast cancer. MATERIALS AND

methodsThe expression level of Sema4D was investigated in MCF10A, 184A1, HCC1937, MDA-MB-468, MDA-MB-231, Hs578T, BT474, MCF-7, and T47D breast cancer cell lines by Western blotting analysis. Sema4D downregulation or overexpression was established by infection with lentiviruses-encoding Sema4D short hairpin RNA (shRNA) or Sema4D. To evaluate the effects of Sema4D on cell proliferation, cell cycle progression, apoptosis, invasion, and migration of MDA-MB-231 and MDA-MB-468 cells, methods including MTT assay, flow cytometry, wound healing assay, and transwell experiments were applied. BALB/c nude mice were injected with MDA-MB-231 cells, which were respectively infected with lentiviruses-encoding Sema4D, Sema4D shRNA, and GFP, followed by tumor angiogenesis assay.

resultsSema4D was expressed at higher levels in breast cancer cell lines compared with the normal human breast epithelial cell lines, especially in MDA-MB-231 and MDA-MB-468 cells. Cell proliferation ability was remarkably inhibited in Sema4D downregulated condition, whereas the proportions of cells in the G0/G1 phase and apoptosis increased in MDA-MB-231 and MDA-MB-468 cells. In addition, the invasion and migration abilities of these cells were obviously reduced. Xenograft growth as well as angiogenesis was inhibited when infected with lentiviruses-encoding Sema4D shRNA in vivo.

conclusionDownregulation of Sema4D had notable influence on cell proliferation ability, invasion, migration, and apoptosis of both MDA-MB-231 and MDA-MB-468 cells. Furthermore, infection with lentiviruses-encoding Sema4D shRNA obviously inhibited tumor growth and angiogenesis in BALB/c nude mice. Our results showed that Sema4D may represent a novel therapeutic target for human breast cancer.

Indexed as

angiogenesisapoptosisbreast cancerproliferationsemaphorin 4D

Identifiers

PMID27729799
PMCPMC5045906
OpenAlexW2527458261

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.