Evidence map›Paper›PMID 30535445›Full record

ArticleOncology reports2019

Hypoxia‑induced galectin‑3 enhances RhoA function to activate the motility of tumor cells in non‑small cell lung cancer.

Yoko Kataoka, Yasuhiko Ohshio, Koji Teramoto, Tomoyuki Igarashi, Tohru Asai, Jun Hanaoka

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

15 citing papers in PubMed, 27 citations in OpenAlex.

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  13. Galectin-3 protects against ischemic stroke by promoting neuro-angiogenesis via apoptosis inhibition and Akt/Caspase regulation.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021
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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 1 institution in 1 country.

Yoko KataokaDepartment of Surgery, Shiga University of Medical Science, Otsu, Shiga 520‑2192, Japan.
Yasuhiko OhshioDepartment of Surgery, Shiga University of Medical Science, Otsu, Shiga 520‑2192, Japan.
Koji TeramotoDepartment of Medical Oncology, Shiga University of Medical Science, Otsu, Shiga 520‑2192, Japan.
Tomoyuki IgarashiDepartment of Surgery, Shiga University of Medical Science, Otsu, Shiga 520‑2192, Japan.
Tohru AsaiDepartment of Surgery, Shiga University of Medical Science, Otsu, Shiga 520‑2192, Japan.
Jun HanaokaDepartment of Surgery, Shiga University of Medical Science, Otsu, Shiga 520‑2192, Japan.
Shiga University of Medical Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Galectin‑3 plays crucial roles in tumor progression. However, in non‑small cell lung cancer (NSCLC), it remains unclear whether the hypoxic tumor microenvironment enhances galectin‑3‑induced cell motility. We investigated galectin‑3 expression in NSCLC cells under hypoxia, and the possible molecular mechanisms by which galectin‑3 influences tumor aggressiveness. Galectin‑3 levels in NSCLC cell lines under hypoxia were assessed using reverse transcription PCR and western blotting. To clarify the role of endogenous galectin‑3, the effect of galectin‑3 knockdown in NSCLC cells was investigated using scratch and invasion assays. The expression and clinicopathological significance of galectin‑3 in 57 patients with pN0M0 invasive pulmonary adenocarcinoma were investigated by immunohistochemistry. Both mRNA and protein levels of galectin‑3 in the NSCLC cell lines A549 and LK‑2 were upregulated by hypoxia. As revealed by scratch and invasion assays, the cell migratory and invasive activities were significantly increased under hypoxia, but were reduced by galectin‑3 knockdown. Notably, addition of galectin‑3 to the media did not improve the cell motility impaired by galectin‑3 knockdown. To clarify the role of endogenous galectin‑3 in the enhancement of tumor cell motility under hypoxia, we focused on the function of RhoA. RhoA level in the plasma membrane, but not in the cytoplasm, was increased under hypoxia and decreased by galectin‑3 knockdown. RhoA activity was significantly enhanced under hypoxia and effectively inhibited by galectin‑3 knockdown. In patients with pN0M0 invasive pulmonary adenocarcinoma, higher galectin‑3 expression on tumor cells was significantly associated with tumor cell invasion into microvessels and tumor recurrence after surgery. These data demonstrate that in NSCLC cells under hypoxia, upregulated galectin‑3 levels increase the localization of RhoA to the plasma membrane, thus enhancing RhoA activity, which is associated with aggressive cell motility. In pN0M0 invasive pulmonary adenocarcinoma, galectin‑3 is a potential biomarker for predicting tumor recurrence after radical surgery.

Indexed as

Adenocarcinoma of LungAgedAged, 80 and overBiomarkers, TumorBlood ProteinsCarcinoma, Non-Small-Cell LungCell HypoxiaCell MembraneCell MovementDisease-Free SurvivalFemaleGalectin 3GalectinsGene Knockdown TechniquesHumansLungBiomarkers, TumorBlood ProteinsGalectin 3GalectinsLGALS3 protein, humanrhoA GTP-Binding ProteinRHOA protein, humanRNA, Messenger

Identifiers

PMID30535445
PMCPMC6312936
OpenAlexW2904922955

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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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.