Evidence map›Paper›PMID 28004467›Full record

ArticleCancer science2017

Podocalyxin influences malignant potential by controlling epithelial-mesenchymal transition in lung adenocarcinoma.

Hidenori Kusumoto, Yasushi Shintani, Ryu Kanzaki, Tomohiro Kawamura, Soichiro Funaki, Masato Minami, Izumi Nagatomo, Eiichi Morii, Meinoshin Okumura

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 2 pooled it
1.7field-weighted citation impact, top 13% 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

19 citing papers in PubMed, 2 syntheses or guidelines pooled it, 26 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

9 authors at 1 institution in 1 country.

Hidenori KusumotoDepartment of General Thoracic Surgery, Osaka University Graduate School of Medicine, Osaka, Japan.
Yasushi ShintaniDepartment of General Thoracic Surgery, Osaka University Graduate School of Medicine, Osaka, Japan.
Ryu KanzakiDepartment of General Thoracic Surgery, Osaka University Graduate School of Medicine, Osaka, Japan.
Tomohiro KawamuraDepartment of General Thoracic Surgery, Osaka University Graduate School of Medicine, Osaka, Japan.
Soichiro FunakiDepartment of General Thoracic Surgery, Osaka University Graduate School of Medicine, Osaka, Japan.
Masato MinamiDepartment of General Thoracic Surgery, Osaka University Graduate School of Medicine, Osaka, Japan.
Izumi NagatomoDepartment of Respiratory Medicine, Allergy and Rheumatic Disease, Osaka University Graduate School of Medicine, Osaka, Japan.
Eiichi MoriiDepartment of Pathology, Osaka University Graduate School of Medicine, Osaka, Japan.
Meinoshin OkumuraDepartment of General Thoracic Surgery, Osaka University Graduate School of Medicine, Osaka, Japan.
Osaka University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial-mesenchymal transition (EMT) plays an important role in the progression of lung carcinoma. Podocalyxin (PODXL), which belongs to the CD34 family and regulates cell morphology, has been linked to EMT in lung cancer, and PODXL overexpression is associated with poor prognosis in several different classes of cancers. The aim of this study was to clarify the role of PODXL overexpression in EMT in lung cancer, and to determine the prognostic value of PODXL overexpression in tumors from lung cancer patients. The morphology, EMT marker expression, and migration and invasion abilities of engineered A549 PODXL-knockdown (KD) or PODXL-overexpression (OE) lung adenocarcinoma cells were examined. PODXL expression levels were assessed by immunohistochemistry in 114 human clinical lung adenocarcinoma specimens and correlated with clinical outcomes. PODXL-KD cells were epithelial in shape, whereas PODXL-OE cells displayed mesenchymal morphology. Epithelial markers were upregulated in PODXL-KD cells and downregulated in PODXL-OE cells, whereas mesenchymal markers were downregulated in the former and upregulated in the latter. A highly selective inhibitor of phosphatidylinositol 3-kinase-Akt signaling attenuated EMT of PODXL-OE cells, while a transforming growth factor inhibitor did not, suggesting that PODXL induces EMT of lung adenocarcinoma cells via the phosphatidylinositol 3-kinase pathway. In lung adenocarcinoma clinical specimens, PODXL expression was detected in minimally invasive and invasive adenocarcinoma, but not in non-invasive adenocarcinoma. Disease free survival and cancer-specific survival were significantly worse for patients whose tumors overexpressed PODXL. PODXL overexpression induces EMT in lung adenocarcinoma and contributes to tumor progression.

Indexed as

A549 CellsAdenocarcinomaAdenocarcinoma of LungCadherinsCell Line, TumorCell MovementDisease-Free SurvivalDisease ProgressionEpithelial-Mesenchymal TransitionHumansLung NeoplasmsNeoplasm InvasivenessPhosphoinositide-3 Kinase InhibitorsRNA InterferenceRNA, Small InterferingSialoglycoproteinsCadherinsPhosphoinositide-3 Kinase InhibitorspodocalyxinRNA, Small InterferingSialoglycoproteinsAktepithelial mesenchymal transitionlung adenocarcinomaphosphatidylinositol 3-kinasepodocalyxin

Identifiers

PMID28004467
PMCPMC5378270
OpenAlexW2562042063

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.