Evidence map›Paper›PMID 28035402›Full record

ArticleOncology reports2017

Transforming growth factor-β1 suppresses bone morphogenetic protein-2-induced mesenchymal-epithelial transition in HSC-4 human oral squamous cell carcinoma cells via Smad1/5/9 pathway suppression.

Takahiro Chiba, Akira Ishisaki, Seiko Kyakumoto, Toshiyuki Shibata, Hiroyuki Yamada, Masaharu Kamo

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.0field-weighted citation impact, top 21% 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

14 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Bone Morphogenic Protein Signaling and Melanoma.Current treatment options in oncology · 2021
    Review
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  9. Article
  10. Article
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  12. 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

6 authors at 2 institutions in 1 country.

Takahiro ChibaDivision of Cellular Biosignal Sciences, Department of Biochemistry, Iwate Medical University, Yahaba-cho, Iwate 028-3694, Japan.
Akira IshisakiDivision of Cellular Biosignal Sciences, Department of Biochemistry, Iwate Medical University, Yahaba-cho, Iwate 028-3694, Japan.
Seiko KyakumotoDivision of Cellular Biosignal Sciences, Department of Biochemistry, Iwate Medical University, Yahaba-cho, Iwate 028-3694, Japan.
Toshiyuki ShibataDepartment of Oral and Maxillofacial Surgery, Gifu University Graduate School of Medicine, Gifu-shi, Gifu 501-1194, Japan.
Hiroyuki YamadaDivision of Oral and Maxillofacial Surgery, Department of Reconstructive Oral and Maxillofacial Surgery, Iwate Medical University School of Dentistry, Morioka, Iwate 020-8505, Japan.
Masaharu KamoDivision of Cellular Biosignal Sciences, Department of Biochemistry, Iwate Medical University, Yahaba-cho, Iwate 028-3694, Japan.
Iwate Medical University · JPGifu University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Squamous cell carcinoma is the most common cancer in the oral cavity. We previously demonstrated that transforming growth factor-β1 (TGF-β1) promotes the epithelial-mesenchymal transition (EMT) of human oral squamous cell carcinoma (hOSCC) cells; however, it remains to be clarified whether the TGF-β superfamily member bone morphogenetic protein (BMP) affects this process in hOSCC cells. Here, we examined the independent and collective effects of TGF-β1 and BMP-2 on EMT and mesenchymal‑epithelial transition (MET) in a panel of four hOSCC cell lines. Notably, we found that HSC-4 cells were the most responsive to BMP-2 stimulation, which resulted in the upregulation of Smad1/5/9 target genes such as the MET inducers ID1 and cytokeratin 9 (CK9). Furthermore, BMP-2 downregulated the mesenchymal marker N-cadherin and the EMT inducer Snail, but upregulated epithelial CK9 expression, indicating that BMP-2 prefers to induce MET rather than EMT. Moreover, TGF-β1 dampened BMP-2-induced epithelial gene expression by inhibiting Smad1/5/9 expression and phosphorylation. Functional analysis revealed that TGF-β1 and BMP-2 significantly enhanced HSC-4 cell migration and proliferation, respectively. Collectively, these data suggest that TGF-β positively regulates hOSCC invasion in the primary tumor, whereas BMP-2 facilitates cancer cell colonization at secondary metastatic sites. Thus, the invasive and metastatic characteristics of hOSCC appear to be reciprocally regulated by BMP and TGF-β.

Indexed as

ApoptosisBlotting, WesternBone Morphogenetic Protein 2Carcinoma, Squamous CellCell MovementCell ProliferationEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansMouth NeoplasmsReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionRNA, MessengerSmad1 ProteinSmad5 ProteinSmad8 ProteinBMP2 protein, humanBone Morphogenetic Protein 2RNA, MessengerSmad1 ProteinSMAD1 protein, humanSmad5 ProteinSMAD5 protein, humanSmad8 ProteinSMAD9 protein, humanSmad ProteinsTransforming Growth Factor beta1

Identifiers

PMID28035402
PMCPMC5355686
OpenAlexW2561728325

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.