Evidence map›Paper›PMID 31387622›Full record

ArticleJournal of experimental & clinical cancer research : CR2019

Depleting PTOV1 sensitizes non-small cell lung cancer cells to chemotherapy through attenuating cancer stem cell traits.

Zhiqiang Wu, Zhuang Liu, Xiangli Jiang, Zeyun Mi, Maobin Meng, Hui Wang, Jinlin Zhao, Boyu Zheng, Zhiyong Yuan

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 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
0.9field-weighted citation impact, top 31% 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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  11. miR-26a-5p Suppresses Wnt/Disease markers · 2022
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  15. Itraconazole Alters the Stem Cell Characteristics of A549 and NCI-H460 Human Lung Cancer Cells by Suppressing Wnt Signaling.Medical science monitor : international medical journal of experimental and clinical research · 2019
    Article
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 2 institutions in 1 country.

Zhiqiang WuDepartment of Radiation Oncology, Tianjin Medical University Cancer Institute & Hospital, Key Laboratory of Cancer Prevention and Therapy, National Clinical Research Center for Cancer, Tianjin's Clinical Research Center for Cancer, Tianjin, 300060, China. zwu08@tmu.edu.cn.ORCID http://orcid.org/0000-0002-1800-9527
Zhuang LiuDepartment of Radiation Oncology, Tianjin Medical University Cancer Institute & Hospital, Key Laboratory of Cancer Prevention and Therapy, National Clinical Research Center for Cancer, Tianjin's Clinical Research Center for Cancer, Tianjin, 300060, China.
Xiangli JiangDepartment of Thoracic Medical Oncology, Tianjin Medical University Cancer Institute & Hospital, Tianjin, 300060, China.
Zeyun MiDepartment of Biochemistry and Molecular Biology, College of Basic Medical Science, Tianjin Medical University, Tianjin, 300070, China.
Maobin MengDepartment of Radiation Oncology, Tianjin Medical University Cancer Institute & Hospital, Key Laboratory of Cancer Prevention and Therapy, National Clinical Research Center for Cancer, Tianjin's Clinical Research Center for Cancer, Tianjin, 300060, China.
Hui WangDepartment of Radiation Oncology, Tianjin Medical University Cancer Institute & Hospital, Key Laboratory of Cancer Prevention and Therapy, National Clinical Research Center for Cancer, Tianjin's Clinical Research Center for Cancer, Tianjin, 300060, China.
Jinlin ZhaoDepartment of Radiation Oncology, Tianjin Medical University Cancer Institute & Hospital, Key Laboratory of Cancer Prevention and Therapy, National Clinical Research Center for Cancer, Tianjin's Clinical Research Center for Cancer, Tianjin, 300060, China.
Boyu ZhengDepartment of Radiation Oncology, Tianjin Medical University Cancer Institute & Hospital, Key Laboratory of Cancer Prevention and Therapy, National Clinical Research Center for Cancer, Tianjin's Clinical Research Center for Cancer, Tianjin, 300060, China.
Zhiyong YuanDepartment of Radiation Oncology, Tianjin Medical University Cancer Institute & Hospital, Key Laboratory of Cancer Prevention and Therapy, National Clinical Research Center for Cancer, Tianjin's Clinical Research Center for Cancer, Tianjin, 300060, China. zyuan@tmu.edu.cn.
Tianjin Medical University Cancer Institute and Hospital · CNTianjin Medical University · CN

Funding

National Natural Science Foundation of China 31700144National Natural Science Foundation of China 81472797National Natural Science Foundation of China 81501988National Natural Science Foundation of China 81502660National Natural Science Foundation of China 81872465Natural Science Foundation of Tianjin Municipal Science and Technology Commission 16JCQNJC10000Natural Science Foundation of Tianjin Municipal Science and Technology Commission 17JCQNJC10600
6 · The paper itself

Abstract

backgroundProstate tumor over expressed gene 1 (PTOV1) has been reported as an oncogene in several human cancers. However, the clinical significance and biological role of PTOV1 remain elusive in non-small cell lung cancer (NSCLC).

methodsThe Cancer Genome Atlas (TCGA) data and NCBI/GEO data mining, western blotting analysis and immunohistochemistry were employed to characterize the expression of PTOV1 in NSCLC cell lines and tissues. The clinical significance of PTOV1 in NSCLC was studied by immunohistochemistry statistical analysis and Kaplan-Meier Plotter database mining. A series of in-vivo and in-vitro assays, including colony formation, CCK-8 assays, flow cytometry, wound healing, trans-well assay, tumor sphere formation, quantitative PCR, gene set enrichment analysis (GSEA), immunostaining and xenografts tumor model, were performed to demonstrate the effects of PTOV1 on chemosensitivity of NSCLC cells and the underlying mechanisms.

resultsPTOV1 is overexpressed in NSCLC cell lines and tissues. High PTOV1 level indicates a short survival time and poor response to chemotherapy of NSCLC patients. Depleting PTOV1 increased sensitivity to chemotherapy drugs cisplatin and docetaxel by increasing cell apoptosis, inhibiting cell migration and invasion. Our study verified that depleting PTOV1 attenuated cancer stem cell traits through impairing DKK1/β-catenin signaling to enhance chemosensitivity of NSCLC cells.

conclusionThese results suggest that PTOV1 plays an important role in the development and progression of human NSCLC and PTOV1 may serve as a therapeutic target for NSCLC patients.

Indexed as

Drug Resistance, NeoplasmAdaptor Proteins, Signal TransducingAnimalsApoptosisBiomarkersBiomarkers, TumorCarcinoma, Non-Small-Cell LungCell Line, TumorCell MovementComputational BiologyDisease Models, AnimalFemaleGene ExpressionGene Expression ProfilingHeterograftsHumansAdaptor Proteins, Signal TransducingBiomarkersBiomarkers, TumorNeoplasm ProteinsPTOV1 protein, humanCancer stem cellChemotherapyNon-small cell lung cancerPTOV1β-Catenin

Identifiers

PMID31387622
PMCPMC6685258
OpenAlexW2966452581

What OpenQuestion holds

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LicenceCC BY
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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.