Evidence map›Paper›PMID 36106406›Full record

ArticleCancer science2023

Hypoxia-induced CXC chemokine ligand 14 expression drives protumorigenic effects through activation of insulin-like growth factor-1 receptor signaling in glioblastoma.

Sung-Tai Wei, Jung-Ying Chiang, Hwai-Lee Wang, Fu-Ju Lei, Yen-Chih Huang, Chi-Chung Wang, Der-Yang Cho, Chia-Hung Hsieh

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.4field-weighted citation impact, top 17% 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

14 citing papers in PubMed, 14 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

8 authors at 3 institutions in 1 country.

Sung-Tai WeiGraduate Institute of Biomedical Sciences, China Medical University, Taichung, Taiwan.
Jung-Ying ChiangGraduate Institute of Biomedical Sciences, China Medical University, Taichung, Taiwan.
Hwai-Lee WangGraduate Institute of Biomedical Sciences, China Medical University, Taichung, Taiwan.
Fu-Ju LeiGraduate Institute of Biomedical Sciences, China Medical University, Taichung, Taiwan.
Yen-Chih HuangGraduate Institute of Biomedical Sciences, China Medical University, Taichung, Taiwan.
Chi-Chung WangGraduate Institute of Biomedical and Pharmaceutical Science, Fu Jen Catholic University, New Taipei, Taiwan.
Der-Yang ChoGraduate Institute of Biomedical Sciences, China Medical University, Taichung, Taiwan.
Chia-Hung HsiehGraduate Institute of Biomedical Sciences, China Medical University, Taichung, Taiwan.ORCID https://orcid.org/0000-0002-4364-0994
China Medical University · TWAsia University · TWFu Jen Catholic University · TW

Funding

China Medical University and Hospital DMR-108-145China Medical University and Hospital DMR-109-114China Medical University and Hospital DMR-109-149China Medical University and Hospital DMR-110-092China Medical University and Hospital DMR-110-149China Medical University and Hospital DMR-110-160China Medical University and Hospital DMR-110-246The Ministry of Science and Technology of the Republic of China 108-2628-B-039-002The Ministry of Science and Technology of the Republic of China MOST 109-2628-B-039-005The Ministry of Science and Technology of the Republic of China MOST 110-2628-B-039-006
6 · The paper itself

Abstract

Hypoxic tumor microenvironment (HTM) promotes a more aggressive and malignant state in glioblastoma. However, little is known about the role and mechanism of CXC chemokine ligand 14 (CXCL14) in HTM-mediated glioblastoma progression. In this study, we report that CXCL14 expression correlated with poor outcomes, tumor grade, and hypoxia-inducible factor (HIF) expression in patients with glioblastoma. CXCL14 was upregulated in tumor cells within the hypoxic areas of glioblastoma. Hypoxia induced HIF-dependent expression of CXCL14, which promoted glioblastoma tumorigenicity and invasiveness in vitro and in vivo. Moreover, CXCL14 gain-of-function in glioblastoma cells activated insulin-like growth factor-1 receptor (IGF-1R) signal transduction to regulate the growth, invasiveness, and neurosphere formation of glioblastoma. Finally, systemic delivery of CXCL14 siRNA nanoparticles (NPs) with polysorbate 80 coating significantly suppressed tumor growth in vivo and extended the survival time in patient-derived glioblastoma xenografts. Together, these findings suggest that HIF-dependent CXCL14 expression contributes to HTM-promoted glioblastoma tumorigenicity and invasiveness through activation of the IGF-1R signaling pathway. CXCL14 siRNA NPs as an oligonucleotide drug can inhibit glioblastoma progression and constitute a translational path for the clinical treatment of glioblastoma patients.

Indexed as

GlioblastomaCell Line, TumorChemokines, CXCHumansHypoxiaInsulin-Like Growth Factor ILigandsRNA, Small InterferingSignal TransductionTumor MicroenvironmentChemokines, CXCInsulin-Like Growth Factor ILigandsRNA, Small InterferingCXC chemokine ligand 14glioblastomahypoxia-inducible factornanoparticletumor hypoxia

Identifiers

PMID36106406
PMCPMC9807529
OpenAlexW4295903203

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.