Evidence map›Paper›PMID 33455947›Full record

ArticleMolecules and cells2021

Expression of HYOU1 via Reciprocal Crosstalk between NSCLC Cells and HUVECs Control Cancer Progression and Chemoresistance in Tumor Spheroids.

Minji Lee, Yeonhwa Song, Inhee Choi, Su-Yeon Lee, Sanghwa Kim, Se-Hyuk Kim, Jiho Kim, Haeng Ran Seo

Abstract read
In one paragraph

Article in Molecules and cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
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

13 citing papers in PubMed.

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  11. Journal of Cancer · 2022
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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

8 authors.

Minji LeeCancer Biology Research Laboratory.ORCID https://orcid.org/0000-0003-3115-3184
Yeonhwa SongCancer Biology Research Laboratory.ORCID https://orcid.org/0000-0002-9616-8726
Inhee ChoiMedicinal Chemistry.ORCID https://orcid.org/0000-0001-7884-1764
Su-Yeon LeeCancer Biology Research Laboratory.ORCID https://orcid.org/0000-0002-5572-1839
Sanghwa KimCancer Biology Research Laboratory.ORCID https://orcid.org/0000-0002-9353-5519
Se-Hyuk KimCancer Biology Research Laboratory.ORCID https://orcid.org/0000-0002-1906-9652
Jiho KimScreening Discovery Platform, Institut Pasteur Korea, Seongnam 13488, Korea.ORCID https://orcid.org/0000-0001-5465-5596
Haeng Ran SeoCancer Biology Research Laboratory.ORCID https://orcid.org/0000-0003-1207-0471

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Among all cancer types, lung cancer ranks highest worldwide in terms of both incidence and mortality. The crosstalk between lung cancer cells and their tumor microenvironment (TME) has begun to emerge as the "Achilles heel" of the disease and thus constitutes an attractive target for anticancer therapy. We previously revealed that crosstalk between lung cancer cells and endothelial cells (ECs) induces chemoresistance in multicellular tumor spheroids (MCTSs). In this study, we demonstrated that factors secreted in response to crosstalk between ECs and lung cancer cells play pivotal roles in the development of chemoresistance in lung cancer spheroids. We subsequently determined that the expression of hypoxia up-regulated protein 1 (HYOU1) in lung cancer spheroids was increased by factors secreted in response to crosstalk between ECs and lung cancer cells. Direct interaction between lung cancer cells and ECs also caused an elevation in the expression of HYOU1 in MCTSs. Inhibition of HYOU1 expression not only suppressed stemness and malignancy, but also facilitated apoptosis and chemosensitivity in lung cancer MCTSs. Inhibition of HYOU1 expression also significantly increased the expression of interferon signaling components in lung cancer cells. Moreover, the activation of the PI3K/AKT/mTOR pathway was involved in the HYOU1-induced aggression of lung cancer cells. Taken together, our results identify HYOU1, which is induced in response to crosstalk between ECs and lung cancer cells within the TME, as a potential therapeutic target for combating the aggressive behavior of cancer cells.

Indexed as

Disease ProgressionDrug Resistance, NeoplasmCarcinoma, Non-Small-Cell LungCell Line, TumorCell ProliferationDown-RegulationEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHSP70 Heat-Shock ProteinsHumansHuman Umbilical Vein Endothelial CellsInterferonsLung NeoplasmsModels, BiologicalNeoplastic Stem CellsPhosphatidylinositol 3-KinasesHSP70 Heat-Shock ProteinsInterferonsMTOR protein, humanoxygen-regulated proteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine Kinaseschemoresistanceendothelial cellshypoxia up-regulated protein 1lung cancermulticellular tumor spheroids

Identifiers

PMID33455947
PMCPMC7854178

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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.