Evidence map›Paper›PMID 34209885›Full record

ArticleCancers2021

Glycyrrhizin Derivatives Suppress Cancer Chemoresistance by Inhibiting Progesterone Receptor Membrane Component 1.

Yasuaki Kabe, Ikko Koike, Tatsuya Yamamoto, Miwa Hirai, Ayaka Kanai, Ryogo Furuhata, Hitoshi Tsugawa, Erisa Harada, Kenji Sugase, Kazue Hanadate and 9 more

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

13 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. HMGB1: A Central Node in Cancer Therapy Resistance.International journal of molecular sciences · 2025
    Review
  3. Review
  4. Review
  5. Review
  6. Sigma Receptors: Novel Regulators of Iron/Heme Homeostasis and Ferroptosis.International journal of molecular sciences · 2023
    Review
  7. Review
  8. Review
  9. Recent Advances inMetabolites · 2022
    Review
  10. Article
  11. Article
  12. Article
  13. 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 8 institutions in 1 country.

Yasuaki KabeDepartment of Biochemistry, Keio University School of Medicine, Tokyo 160-8582, Japan.ORCID 0000-0003-0952-011X
Ikko KoikeDepartment of Biochemistry, Keio University School of Medicine, Tokyo 160-8582, Japan.
Tatsuya YamamotoBioorganic Research Institute, Suntory Foundation for Life Sciences (SUNBOR), 8-1-1 Seikadai, Seika, Soraku, Kyoto 619-0284, Japan.
Miwa HiraiDepartment of Biochemistry, Keio University School of Medicine, Tokyo 160-8582, Japan.
Ayaka KanaiDepartment of Biochemistry, Keio University School of Medicine, Tokyo 160-8582, Japan.
Ryogo FuruhataDepartment of Biochemistry, Keio University School of Medicine, Tokyo 160-8582, Japan.
Hitoshi TsugawaDepartment of Biochemistry, Keio University School of Medicine, Tokyo 160-8582, Japan.ORCID 0000-0002-4344-4475
Erisa HaradaBioorganic Research Institute, Suntory Foundation for Life Sciences (SUNBOR), 8-1-1 Seikadai, Seika, Soraku, Kyoto 619-0284, Japan.
Kenji SugaseDepartment of Molecular Engineering, Graduate School of Engineering, Kyoto University, Kyoto-Daigaku Katsura, Nishikyo-Ku, Kyoto 615-8510, Japan.ORCID 0000-0001-8623-7743
Kazue HanadateCokey, Co., Ltd., 2 Sanbancho, Chiyoda-ku, Tokyo 102-0075, Japan.
Nobuji YoshikawaCokey, Co., Ltd., 2 Sanbancho, Chiyoda-ku, Tokyo 102-0075, Japan.ORCID 0000-0002-8093-9098
Hiroaki HayashiLaboratory of Natural Products Chemistry, College of Pharmaceutical Sciences, Ritsumeikan University, 1-1-1 Nojihigashi, Kusatsu, Shiga 525-8577, Japan.
Masanori NodaU-Medico Inc., Osaka 565-0871, Japan.
Susumu UchiyamaDepartment of Biotechnology, Graduate School of Engineering, Osaka University, Osaka 565-0871, Japan.ORCID 0000-0002-5181-179X
Hiroki YamazakiDepartment of Rheumatology and Allergy, IMSUT Hospital, The Institute of Medical Science, The University of Tokyo 108-8639, Japan.
Hirotoshi TanakaDepartment of Rheumatology and Allergy, IMSUT Hospital, The Institute of Medical Science, The University of Tokyo 108-8639, Japan.
Takuya KobayashiDepartment of Medical Chemistry, Kansai Medical University, Hirakata, Osaka 573-1010, Japan.
Hiroshi HandaDepartment of Chemical Biology, Tokyo Medical University, Tokyo 160-8402, Japan.ORCID 0000-0001-6656-9521
Makoto SuematsuDepartment of Biochemistry, Keio University School of Medicine, Tokyo 160-8582, Japan.
Keio University · JPSuntory Foundation for Life Sciences · JPUniversity of Tokyo Hospital · JPKansai Medical University · JPKyoto University · JPRitsumeikan University · JPThe University of Osaka · JPTokyo Medical University · JP

Funding

AMED-CREST JP17gm0710010JSPS KAKENHI 18K06921JST Moonshot R&D JPMJPS2022
6 · The paper itself

Abstract

Progesterone receptor membrane component 1 (PGRMC1) is highly expressed in various cancer cells and contributes to tumor progression. We have previously shown that PGRMC1 forms a unique heme-stacking functional dimer to enhance EGF receptor (EGFR) activity required for cancer proliferation and chemoresistance, and the dimer dissociates by carbon monoxide to attenuate its biological actions. Here, we determined that glycyrrhizin (GL), which is conventionally used to ameliorate inflammation, specifically binds to heme-dimerized PGRMC1. Binding analyses using isothermal titration calorimetry revealed that some GL derivatives, including its glucoside-derivative (GlucoGL), bind to PGRMC1 potently, whereas its aglycone, glycyrrhetinic acid (GA), does not bind. GL and GlucoGL inhibit the interaction between PGRMC1 and EGFR, thereby suppressing EGFR-mediated signaling required for cancer progression. GL and GlucoGL significantly enhanced EGFR inhibitor erlotinib- or cisplatin (CDDP)-induced cell death in human colon cancer HCT116 cells. In addition, GL derivatives suppressed the intracellular uptake of low-density lipoprotein (LDL) by inhibiting the interaction between PGRMC1 and the LDL receptor (LDLR). Effects on other pathways cannot be excluded. Treatment with GlucoGL and CDDP significantly suppressed tumor growth following xenograft transplantation in mice. Collectively, this study indicates that GL derivatives are novel inhibitors of PGRMC1 that suppress cancer progression, and our findings provide new insights for cancer treatment.

Indexed as

chemoresistanceEGF receptorendocytosisglycyrrhizinglycyrrhizin derivativeslow-density lipoproteinprogesterone receptor membrane component 1

Identifiers

PMID34209885
PMCPMC8269059
OpenAlexW3173855973

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.