Evidence map›Paper›PMID 32756527›Full record

ArticleCells2020

NDAT Targets PI3K-Mediated PD-L1 Upregulation to Reduce Proliferation in Gefitinib-Resistant Colorectal Cancer.

Tung-Yung Huang, Tung-Cheng Chang, Yu-Tang Chin, Yi-Shin Pan, Wong-Jin Chang, Feng-Cheng Liu, Ema Dwi Hastuti, Shih-Jiuan Chiu, Shwu-Huey Wang, Chun A Changou and 11 more

Open access · goldAbstract read
In one paragraph

Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.8field-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

23 citing papers in PubMed, 29 citations in OpenAlex.

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  13. The power of heteronemin in cancers.Journal of biomedical science · 2022
    Review
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  18. Review
  19. Review
  20. Regulatory mechanisms of immune checkpoints PD-L1 and CTLA-4 in cancer.Journal of experimental & clinical cancer research : CR · 2021
    Review
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

21 authors at 7 institutions in 2 countries.

Tung-Yung HuangGraduate Institute of Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei 11031, Taiwan.
Tung-Cheng ChangDivision of Colorectal Surgery, Department of Surgery, Taipei Medical University Shuang Ho Hospital, New Taipei City 235041, Taiwan.
Yu-Tang ChinSchool of Dentistry, Taipei Medical University, Taipei 11031, Taiwan.
Yi-Shin PanGraduate Institute of Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei 11031, Taiwan.
Wong-Jin ChangGraduate Institute of Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei 11031, Taiwan.ORCID 0000-0002-5453-8856
Feng-Cheng LiuDivision of Rheumatology, Immunology, and Allergy, Tri-Service General Hospital, Taipei 114, Taiwan.
Ema Dwi HastutiSchool of Pharmacy, College of Pharmacy, Taipei Medical University, Taipei 11031, Taiwan.ORCID 0000-0003-1779-2326
Shih-Jiuan ChiuSchool of Pharmacy, College of Pharmacy, Taipei Medical University, Taipei 11031, Taiwan.ORCID 0000-0001-9952-4055
Shwu-Huey WangDepartment of Biochemistry and Molecular Cell Biology, College of Medicine, Taipei Medical University, Taipei 11031, Taiwan.
Chun A ChangouCore Facility Center, Department of Research Development, Taipei Medical University, Taipei 11031, Taiwan.
Zi-Lin LiGraduate Institute of Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei 11031, Taiwan.
Yi-Ru ChenGraduate Institute of Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei 11031, Taiwan.
Hung-Ru ChuGraduate Institute of Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei 11031, Taiwan.
Ya-Jung ShihGraduate Institute of Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei 11031, Taiwan.
R Holland ChengDepartment of Molecular and Cellular Biology, College of Biological Sciences, University of California, Davis, CA 95616, USA.ORCID 0000-0002-2068-7271
Alexander WuThe Ph.D. Program for Translational Medicine, College of Medical Science and Technology, Taipei Medical University, Taipei 110, Taiwan.ORCID 0000-0002-0178-6530
Hung-Yun LinGraduate Institute of Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei 11031, Taiwan.
Kuan WangGraduate Institute of Nanomedicine and Medical Engineering, College of Medical Engineering, Taipei Medical University, Taipei 11031, Taiwan.
Jacqueline Whang-PengGraduate Institute of Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei 11031, Taiwan.
Shaker A MousaPharmaceutical Research Institute, Albany College of Pharmacy and Health Sciences, Albany, NY 12208, USA.ORCID 0000-0002-9294-015X
Paul J DavisPharmaceutical Research Institute, Albany College of Pharmacy and Health Sciences, Albany, NY 12208, USA.ORCID 0000-0002-6794-4917
Taipei Medical University · TWAlbany College of Pharmacy and Health Sciences · USTaipei Medical University Hospital · TWTaipei Medical University-Shuang Ho Hospital · TWTri-Service General Hospital · TWUniversity of California, Davis · USWan Fang Hospital · TW

Funding

Cell-specific nanocarrier with endocytic and endosomolytic activities for therapeutic genome editingUG3TR002866 · NCATS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHENG, R.HOLLAND, LAM, KIT S · 2019 to 2021
$2.3M
NCATS NIH HHS UG3 TR002866
6 · The paper itself

Abstract

The property of drug-resistance may attenuate clinical therapy in cancer cells, such as chemoresistance to gefitinib in colon cancer cells. In previous studies, overexpression of PD-L1 causes proliferation and metastasis in cancer cells; therefore, the PD-L1 pathway allows tumor cells to exert an adaptive resistance mechanism in vivo. Nano-diamino-tetrac (NDAT) has been shown to enhance the anti-proliferative effect induced by first-line chemotherapy in various types of cancer, including colorectal cancer (CRC). In this work, we attempted to explore whether NDAT could enhance the anti-proliferative effect of gefitinib in CRC and clarified the mechanism of their interaction. The MTT assay was utilized to detect a reduction in cell proliferation in four primary culture tumor cells treated with gefitinib or NDAT. The gene expression of

Indexed as

AnimalsAntineoplastic AgentsB7-H1 AntigenCell ProliferationColorectal NeoplasmsDrug Resistance, NeoplasmGefitinibGene Expression Regulation, NeoplasticHCT116 CellsHT29 CellsHumansMicePhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsPolyglactin 910ThyroxineAntineoplastic AgentsB7-H1 AntigenCD274 protein, humanGefitinibnano-diamino-tetracPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsPolyglactin 910Thyroxinecolorectal cancer (CRC)gefitinibNDATPD-L1PI3K

Identifiers

PMID32756527
PMCPMC7464180
OpenAlexW3046624939

What OpenQuestion holds

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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.