Evidence map›Paper›PMID 32789182›Full record

ArticleScience advances2020

Development of a pH-responsive polymersome inducing endoplasmic reticulum stress and autophagy blockade.

Funeng Xu, Xilin Li, Xuehui Huang, Jingmei Pan, Yi Wang, Shaobing Zhou

Open access · goldAbstract read
In one paragraph

Article in Science advances, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
7.0field-weighted citation impact, top 2% 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

25 citing papers in PubMed, 95 citations in OpenAlex.

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  16. Multipotent Poly(Tertiary Amine-Oxide) Micelles for Efficient Cancer Drug Delivery.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022
    Article
  17. Review
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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.

Funeng XuKey Laboratory of Advanced Technologies of Materials, Ministry of Education School of Materials Science and Engineering, Southwest Jiaotong University, Chengdu 610031, China.ORCID 0000-0002-0377-9246
Xilin LiKey Laboratory of Advanced Technologies of Materials, Ministry of Education School of Materials Science and Engineering, Southwest Jiaotong University, Chengdu 610031, China.ORCID 0000-0001-5550-4896
Xuehui HuangKey Laboratory of Advanced Technologies of Materials, Ministry of Education School of Materials Science and Engineering, Southwest Jiaotong University, Chengdu 610031, China.ORCID 0000-0001-8818-9095
Jingmei PanKey Laboratory of Advanced Technologies of Materials, Ministry of Education School of Materials Science and Engineering, Southwest Jiaotong University, Chengdu 610031, China.
Yi WangSchool of Life Science and Engineering, Southwest Jiaotong University, Chengdu 610031, China.
Shaobing ZhouKey Laboratory of Advanced Technologies of Materials, Ministry of Education School of Materials Science and Engineering, Southwest Jiaotong University, Chengdu 610031, China.ORCID 0000-0002-6155-4010
Southwest Jiaotong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is involved in the occurrence and development of tumors. Here, a pH-responsive polymersome codelivering hydroxychloroquine (HCQ) and tunicamycin (Tuni) drugs is developed to simultaneously induce endoplasmic reticulum (ER) stress and autophagic flux blockade for achieving an antitumor effect and inhibiting tumor metastasis. The pH response of poly(β-amino ester) and HCQ synergistically deacidifies the lysosomes, thereby blocking the fusion of autophagosomes and lysosomes and lastly blocking autophagic flux. The function mechanism of regulating autophagy was systematically investigated on orthotopic luciferase gene-transfected, 4T1 tumor-bearing BALB/c mice through Western blot and immunohistochemistry analyses. The Tuni triggers ER stress to regulate the PERK/Akt signaling pathway to increase the autophagic level. The "autophagic stress" generated by triggering ER stress-induced autophagy and blocking autophagic flux is effective against tumors. The reduced expression of matrix metalloproteinase-2 due to ER stress and reduced focal adhesions turnover due to the blockade of autophagic flux synergistically inhibit tumor metastasis.

Identifiers

PMID32789182
PMCPMC7399484
OpenAlexW3046671436

What OpenQuestion holds

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LicenceCC BY-NC
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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.