Evidence map›Paper›PMID 30887707›Full record

ArticleJournal of cellular and molecular medicine2019

FAM3C-YY1 axis is essential for TGFβ-promoted proliferation and migration of human breast cancer MDA-MB-231 cells via the activation of HSF1.

Weili Yang, Biaoqi Feng, Yuhong Meng, Junpei Wang, Bin Geng, Qinghua Cui, Hongquan Zhang, Yang Yang, Jichun Yang

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

40 citing papers in PubMed, 58 citations in OpenAlex.

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  19. Neutrophils promote tumor invasionInternational journal of biological sciences · 2023
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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

9 authors at 3 institutions in 2 countries.

Weili YangKey Laboratory of Molecular Cardiovascular Sciences of the Ministry of Education, Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Center for Non-coding RNA Medicine, Peking University Health Science Center, Beijing, China.
Biaoqi FengKey Laboratory of Molecular Cardiovascular Sciences of the Ministry of Education, Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Center for Non-coding RNA Medicine, Peking University Health Science Center, Beijing, China.
Yuhong MengKey Laboratory of Molecular Cardiovascular Sciences of the Ministry of Education, Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Center for Non-coding RNA Medicine, Peking University Health Science Center, Beijing, China.
Junpei WangKey Laboratory of Molecular Cardiovascular Sciences of the Ministry of Education, Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Center for Non-coding RNA Medicine, Peking University Health Science Center, Beijing, China.
Bin GengState Key Laboratory of Cardiovascular Disease, Hypertension Center, Fuwai Hospital, Peking University Health Science Center, CAMS & PUMC, Beijing, China.
Qinghua CuiKey Laboratory of Molecular Cardiovascular Sciences of the Ministry of Education, Department of Biomedical Informatics, School of Basic Medical Sciences, Center for Non-coding RNA Medicine, Peking University Health Science Center, Beijing, China.
Hongquan ZhangKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), and State Key Laboratory of Natural and Biomimetic Drugs, Peking University Health Science Center, Beijing, China.
Yang YangDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China.
Jichun YangKey Laboratory of Molecular Cardiovascular Sciences of the Ministry of Education, Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Center for Non-coding RNA Medicine, Peking University Health Science Center, Beijing, China.ORCID 0000-0001-8150-2923
Peking University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNMinistry of Education of the People's Republic of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Family with sequence similarity three member C (FAM3C) (interleukin-like EMT inducer [ILEI]), heat shock factor 1 (HSF1) and Ying-Yang 1 (YY1) have been independently reported to be involved in the pathogenesis of various cancers. However, whether they are coordinated to trigger the development of cancer remains unknown. This study determined the role and mechanism of YY1 and HSF1 in FAM3C-induced proliferation and migration of breast cancer cells. In human MDA-MB-231 breast cancer cell line, transforming growth factor-β (TGFβ) up-regulated FAM3C, HSF1 and YY1 expressions. FAM3C overexpression promoted the proliferation and migration of MDA-MB-231 cells with YY1 and HSF1 up-regulation, whereas FAM3C silencing exerted the opposite effects. FAM3C inhibition repressed TGFβ-induced HSF1 activation, and proliferation and migration of breast cancer cells. YY1 was shown to directly activate HSF1 transcription to promote the proliferation and migration of breast cancer cells. YY1 silencing blunted FAM3C- and TGFβ-triggered activation of HSF1-Akt-Cyclin D1 pathway, and proliferation and migration of breast cancer cells. Inhibition of HSF1 blocked TGFβ-, FAM3C- and YY1-induced proliferation and migration of breast cancer cells. YY1 and HSF1 had little effect on FAM3C expression. Similarly, inhibition of HSF1 also blunted FAM3C- and TGFβ-promoted proliferation and migration of human breast cancer BT-549 cells. In human breast cancer tissues, FAM3C, YY1 and HSF1 protein expressions were increased. In conclusion, FAM3C activated YY1-HSF1 signalling axis to promote the proliferation and migration of breast cancer cells. Furthermore, novel FAM3C-YY1-HSF1 pathway plays an important role in TGFβ-triggered proliferation and migration of human breast cancer MDA-MB-231 cells.

Indexed as

Cell MovementSignal TransductionBreast NeoplasmsCell Line, TumorCell ProliferationCytokinesFemaleGene SilencingHeat Shock Transcription FactorsHumansNeoplasm ProteinsTransforming Growth Factor betaUp-RegulationYY1 Transcription FactorCytokinesFAM3C protein, humanHeat Shock Transcription FactorsHSF1 protein, humanNeoplasm ProteinsTransforming Growth Factor betaYY1 protein, humanYY1 Transcription Factorbreast cancerFAM3CHSF1YY1

Identifiers

PMID30887707
PMCPMC6484506
OpenAlexW2923426424

What Socratic 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 Socratic graph.