Evidence map›Paper›PMID 29360662›Full record

ArticleAnti-cancer drugs2018

FoxM1 promotes epithelial-mesenchymal transition, invasion, and migration of tongue squamous cell carcinoma cells through a c-Met/AKT-dependent positive feedback loop.

Huiling Yang, Li Wen, Mingling Wen, Tao Liu, Lisheng Zhao, Bo Wu, Yuyu Yun, Wenchao Liu, Hao Wang, Yu Wang and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Anti-cancer drugs, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 15% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

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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

11 authors at 5 institutions in 1 country.

Huiling YangInstitute of Stomatology, Chinese PLA General Hospital.
Li WenInstitute of Stomatology, Chinese PLA General Hospital.
Mingling WenDepartment of Pharmacy, Affiliated Hospital of Academy of Military Medical Sciences.
Tao LiuDepartment of Stomatology, First Affiliated Hospital of PLA General Hospital, Beijing.
Lisheng ZhaoInstitute of Stomatology, Chinese PLA General Hospital.
Bo WuState Key Laboratory of Cancer Biology, Department of Cell Biology, Cell Engineering Research Center, The Fourth Military Medical University.
Yuyu YunState Key Laboratory of Cancer Biology, Department of Cell Biology, Cell Engineering Research Center, The Fourth Military Medical University.
Wenchao LiuDepartment of Oncology, State Key Discipline of Cell Biology, Xijing Hospital, The Fourth Military Medical University, Xi'an, Shaanxi Province, China.
Hao WangDepartment of Stomatology, Beijing Tiantan Hospital, Capital Medical University.
Yu WangInstitute of Stomatology, Chinese PLA General Hospital.
Ning WenInstitute of Stomatology, Chinese PLA General Hospital.
Chinese PLA General Hospital · CNAir Force Medical University · CNCapital Medical University · CNAcademy of Military Medical Sciences · CNFirst Affiliated Hospital of Chinese PLA General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Forkhead box protein M1 (FoxM1) has been associated with cancer progression and metastasis. However, the function of FoxM1 in tongue squamous cell carcinoma (TSCC) remains largely unknown. The purpose of this study was to determine the role of FoxM1 in regulation of epithelial-mesenchymal transition (EMT) and migration of TSCC cells. We found that FoxM1 induced EMT and increased invasion/migration capacity in SCC9 and SCC25 cells. FoxM1 stimulation increased c-Met, pAKT, and vimentin levels but decreased E-cadherin level. Chromatin immunoprecipitation assay established that FoxM1 is bound to the promoter of c-Met to activate its transcription. In turn, c-Met promoted the expression of FoxM1 and pAKT. Blocking AKT signaling attenuated the invasion and migration of SCC9 and SCC25 cells stimulated by FoxM1 or c-Met. These results indicate that a positive feedback loop controls the EMT and migration of TSCC cells induced by FoxM1 and c-Met through AKT. Furthermore, the expression levels of FoxM1, pAKT, and c-Met were found to significantly increase in TSCC tissues compared with normal tissues, and these three biomarkers were concomitantly expressed in TSCC tissues. Clinical association analyses indicated that the expression of FoxM1, c-Met, and pAKT was associated with clinicopathological characteristics of patients with TSCC including tumor stage, tumor size, and lymph node metastasis. Taken together, our findings suggest that FoxM1 promotes the EMT, invasion and migration of TSCC cells, and cross-talks with c-Met/AKT signaling to form a positive feedback loop to promote TSCC development.

Indexed as

Carcinoma, Squamous CellCell Line, TumorCell MovementEpithelial-Mesenchymal TransitionFeedback, PhysiologicalForkhead Box Protein M1Head and Neck NeoplasmsHumansNeoplasm InvasivenessProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-metSignal TransductionSquamous Cell Carcinoma of Head and NeckTongue NeoplasmsForkhead Box Protein M1FOXM1 protein, humanMET protein, humanProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-met

Identifiers

PMID29360662
PMCPMC5821477
OpenAlexW2790834505

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.