Evidence map›Paper›PMID 29426357›Full record

ArticleJournal of experimental & clinical cancer research : CR2018

14, 15-EET induces breast cancer cell EMT and cisplatin resistance by up-regulating integrin αvβ3 and activating FAK/PI3K/AKT signaling.

Jing Luo, Jian-Feng Yao, Xiao-Fei Deng, Xiao-Dan Zheng, Min Jia, Yue-Qin Wang, Yan Huang, Jian-Hua Zhu

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers.

0numbers the graph read from it
0cells of the map it votes in
123citing papers in PubMed
8.9field-weighted citation impact, top 1% 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

123 citing papers in PubMed, 184 citations in OpenAlex.

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63 more citing papers are in PubMed but not listed here.

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 3 institutions in 1 country.

Jing LuoDepartment of Immunology, Tongji Medical College, Huazhong University of Science and Technology (HUST), Wuhan, Hubei, People's Republic of China.
Jian-Feng YaoQuanzhou Maternal and Child Health Care Hospital, Quanzhou, People's Republic of China.
Xiao-Fei DengDepartment of Immunology, Tongji Medical College, Huazhong University of Science and Technology (HUST), Wuhan, Hubei, People's Republic of China.
Xiao-Dan ZhengDepartment of Radiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology (HUST), Wuhan, Hubei, People's Republic of China.
Min JiaLaboratory of Clinical Immunology, Wuhan No.1 Hospital, Tongji Medical College, Huazhong University of Science and Technology (HUST), 215 Zhongshan Dadao, Wuhan, Hubei, 430022, People's Republic of China.
Yue-Qin WangLaboratory of Clinical Immunology, Wuhan No.1 Hospital, Tongji Medical College, Huazhong University of Science and Technology (HUST), 215 Zhongshan Dadao, Wuhan, Hubei, 430022, People's Republic of China.
Yan HuangLaboratory of Clinical Immunology, Wuhan No.1 Hospital, Tongji Medical College, Huazhong University of Science and Technology (HUST), 215 Zhongshan Dadao, Wuhan, Hubei, 430022, People's Republic of China.
Jian-Hua ZhuLaboratory of Clinical Immunology, Wuhan No.1 Hospital, Tongji Medical College, Huazhong University of Science and Technology (HUST), 215 Zhongshan Dadao, Wuhan, Hubei, 430022, People's Republic of China. zhujh621@163.com.
Huazhong University of Science and Technology · CNWuhan No.1 Hospital · CNTongji Hospital · CN

Funding

China Postdoctoral Science Foundation 2016M602311National Natural Science Foundation of China 81502222Natural Science Foundation of Hubei Province 2013CFB370
6 · The paper itself

Abstract

background14,15-epoxyeicosatrienoic acid (14,15-EET) is an important lipid signaling molecule involved in the regulation of tumor metastasis, however, the role and molecular mechanisms of 14,15-EET activity in breast cancer cell epithelial-mesenchymal transition (EMT) and drug resistance remain enigmatic.

methodsThe 14, 15-EET level in serum and in tumor or non-cancerous tissue from breast cancer patients was measured by ELISA. qRT-PCR and western blot analyses were used to examine expression of integrin αvβ3. The role of 14, 15-EET in breast cancer cell adhesion, invasion was explored by adhesion and Transwell assays. The role of 14, 15-EET in breast cancer cell cisplatin resistance in vitro was determined by MTT assay. Western blot was conducted to detect the protein expressions of EMT-related markers and FAK/PI3K/AKT signaling. Xenograft models in nude mice were established to explore the roles of 14, 15-EET in breast cancer cells EMT and cisplatin resistance in vivo.

resultsIn the present study, we show that serum level of 14, 15-EET increases in breast cancer patients and 14, 15-EET level of tumor tissue is higher than that of non-cancerous tissue. Moreover, 14, 15-EET increases integrin αvβ3 expression, leading to FAK activation. 14, 15-EET induces breast cancer cell EMT via integrin αvβ3 and FAK/PI3K/AKT cascade activation in vitro. Furthermore, we find that 14, 15-EET induces breast cancer cells EMT and cisplatin resistance in vivo, αvβ3 integrin and the resulting FAK/PI3K/AKT signaling pathway are responsible for 14, 15-EET induced-breast cancer cells cisplatin resistance.

conclusionsOur findings suggest that inhibition of 14, 15-EET or inactivation of integrin αvβ3/FAK/PI3K/AKT pathway could serve as a novel approach to reverse EMT and cisplatin resistance in breast cancer cells.

Indexed as

8,11,14-Eicosatrienoic AcidAnimalsBreast NeoplasmsCell AdhesionCell Line, TumorCell MovementCell ProliferationCisplatinDisease Models, AnimalDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionFemaleHumansImmunohistochemistryIntegrin alphaVbeta3Mice14,15-epoxy-5,8,11-eicosatrienoic acid8,11,14-Eicosatrienoic AcidCisplatinIntegrin alphaVbeta3Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt14, 15-EETBreast cancerCisplatin resistanceEMTαvβ3/FAK/PI3K/AKT signaling

Identifiers

PMID29426357
PMCPMC5807756
OpenAlexW2795478721

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.