Evidence map›Paper›PMID 32860290›Full record

ArticleCancer science2020

Chaperone-mediated autophagy receptor modulates tumor growth and chemoresistance in non-small cell lung cancer.

Akihiro Ichikawa, Yu Fujita, Yusuke Hosaka, Tsukasa Kadota, Akihiko Ito, Shigehiro Yagishita, Naoaki Watanabe, Shota Fujimoto, Hironori Kawamoto, Nayuta Saito and 9 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 8% 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, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. Pooled it
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  8. Article
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  13. Insight into autophagy in platinum resistance of cancer.International journal of clinical oncology · 2023
    Review
  14. Review
  15. Article
  16. A perspective on the role of autophagy in cancer.Biochimica et biophysica acta. Molecular basis of disease · 2021
    Review
  17. Article
  18. Article
  19. Review
  20. AQP3-mediated HCancer science · 2021
    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

19 authors at 4 institutions in 2 countries.

Akihiro IchikawaDepartment of Internal Medicine, Division of Respiratory Diseases, The Jikei University School of Medicine, Tokyo, Japan.
Yu FujitaDepartment of Internal Medicine, Division of Respiratory Diseases, The Jikei University School of Medicine, Tokyo, Japan.ORCID https://orcid.org/0000-0002-8916-7303
Yusuke HosakaDepartment of Internal Medicine, Division of Respiratory Diseases, The Jikei University School of Medicine, Tokyo, Japan.
Tsukasa KadotaDepartment of Internal Medicine, Division of Respiratory Diseases, The Jikei University School of Medicine, Tokyo, Japan.
Akihiko ItoDepartment of Internal Medicine, Division of Respiratory Diseases, The Jikei University School of Medicine, Tokyo, Japan.
Shigehiro YagishitaDivision of Molecular Pharmacology, National Cancer Center Research Institute, Tokyo, Japan.
Naoaki WatanabeDepartment of Internal Medicine, Division of Respiratory Diseases, The Jikei University School of Medicine, Tokyo, Japan.
Shota FujimotoDepartment of Internal Medicine, Division of Respiratory Diseases, The Jikei University School of Medicine, Tokyo, Japan.
Hironori KawamotoDepartment of Internal Medicine, Division of Respiratory Diseases, The Jikei University School of Medicine, Tokyo, Japan.
Nayuta SaitoDepartment of Internal Medicine, Division of Respiratory Diseases, The Jikei University School of Medicine, Tokyo, Japan.
Masahiro YoshidaDepartment of Internal Medicine, Division of Respiratory Diseases, The Jikei University School of Medicine, Tokyo, Japan.
Mitsuo HashimotoDepartment of Internal Medicine, Division of Respiratory Diseases, The Jikei University School of Medicine, Tokyo, Japan.
Shunsuke MinagawaDepartment of Internal Medicine, Division of Respiratory Diseases, The Jikei University School of Medicine, Tokyo, Japan.
Hiromichi HaraDepartment of Internal Medicine, Division of Respiratory Diseases, The Jikei University School of Medicine, Tokyo, Japan.
Noriko MotoiDepartment of Diagnostic Pathology, National Cancer Center Hospital, Tokyo, Japan.ORCID https://orcid.org/0000-0001-7098-3311
Yusuke YamamotoDivision of Cellular Signaling, National Cancer Center Research Institute, Tokyo, Japan.ORCID https://orcid.org/0000-0002-5262-8479
Takahiro OchiyaDivision of Molecular and Cellular Medicine, National Cancer Center Research Institute, Tokyo, Japan.ORCID https://orcid.org/0000-0002-0776-9918
Jun ArayaDepartment of Internal Medicine, Division of Respiratory Diseases, The Jikei University School of Medicine, Tokyo, Japan.
Kazuyoshi KuwanoDepartment of Internal Medicine, Division of Respiratory Diseases, The Jikei University School of Medicine, Tokyo, Japan.
Jikei University School of Medicine · JPNational Cancer Research Institute · GBTokyo Medical University · JPTokyo National Hospital · JP

Funding

Japan Society for the Promotion of Science KAKENHI JP17K09672Japan Society for the Promotion of Science KAKENHI JP17K09673Japan Society for the Promotion of Science KAKENHI JP17K09674Japan Society for the Promotion of Science KAKENHI JP18K08158Japan Society for the Promotion of Science KAKENHI JP19K08612Japan Society for the Promotion of Science KAKENHI JP19K08632Japan Society for the Promotion of Science KAKENHI JP19K17649National Cancer Center Research and Development Fund, Japan
6 · The paper itself

Abstract

Chaperone-mediated autophagy (CMA) is a lysosomal degradation pathway of selective soluble proteins. Lysosome-associated membrane protein type 2a (LAMP2A) is the key receptor protein of CMA; downregulation of LAMP2A leads to CMA blockade. Although CMA activation has been involved in cancer growth, CMA status and functions in non-small cell lung cancer (NSCLC) by focusing on the roles in regulating chemosensitivity remain to be clarified. In this study, we found that LAMP2A expression is elevated in NSCLC cell lines and patient's tumors, conferring poor survival and platinum resistance in NSCLC patients. LAMP2A knockdown in NSCLC cells suppressed cell proliferation and colony formation and increased the sensitivity to chemotherapeutic drugs in vitro. Furthermore, we found that intrinsic apoptosis signaling is the mechanism of cell death involved with CMA blockade. Remarkably, LAMP2A knockdown repressed tumorigenicity and sensitized the tumors to cisplatin treatment in NSCLC-bearing mice. Our discoveries suggest that LAMP2A is involved in the regulation of cancer malignant phenotypes and represents a promising new target against chemoresistant NSCLC.

Indexed as

Drug Resistance, NeoplasmSignal TransductionAnimalsApoptosisBiomarkers, TumorCarcinoma, Non-Small-Cell LungCell Line, TumorCell ProliferationGene ExpressionGene Knockdown TechniquesHumansImmunohistochemistryLung NeoplasmsLysosomal-Associated Membrane Protein 2LysosomesPrognosisBiomarkers, TumorLAMP2 protein, humanLysosomal-Associated Membrane Protein 2apoptosischaperone-mediated autophagychemoresistanceLAMP2Alung cancer

Identifiers

PMID32860290
PMCPMC7648026
OpenAlexW3082704790

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.