Evidence map›Paper›PMID 35343027›Full record

ArticleCancer science2022

Blocking cholesterol efflux mechanism is a potential target for antilymphoma therapy.

Hiromu Yano, Yukio Fujiwara, Hasita Horlad, Chang Pan, Keitaro Kai, Daisuke Niino, Kumiko Ohsawa, Morihiro Higashi, Kisato Nosaka, Yutaka Okuno and 4 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

15 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. 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

14 authors at 3 institutions in 1 country.

Hiromu YanoDepartment of Cell Pathology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Yukio FujiwaraDepartment of Cell Pathology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.ORCID https://orcid.org/0000-0002-2074-0597
Hasita HorladDepartment of Cell Pathology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Chang PanDepartment of Cell Pathology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Keitaro KaiDepartment of Neurosurgery, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Daisuke NiinoDepartment of Pathology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan.
Kumiko OhsawaDepartment of Pathology, Saitama Medical Center, Saitama Medical University, Kawagoe, Japan.
Morihiro HigashiDepartment of Pathology, Saitama Medical Center, Saitama Medical University, Kawagoe, Japan.
Kisato NosakaDepartment of Hematology, Rhaumatology, and Infectious Diseases, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.ORCID https://orcid.org/0000-0001-6682-2451
Yutaka OkunoDepartment of Hematology, Rhaumatology, and Infectious Diseases, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Jun-Ichi TamaruDepartment of Pathology, Saitama Medical Center, Saitama Medical University, Kawagoe, Japan.
Akitake MukasaDepartment of Neurosurgery, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Masao MatsuokaDepartment of Hematology, Rhaumatology, and Infectious Diseases, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.ORCID https://orcid.org/0000-0002-0473-754X
Yoshihiro KomoharaDepartment of Cell Pathology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.ORCID https://orcid.org/0000-0001-9723-0846
Kumamoto University · JPSocial Insurance Saitama Chuo Hospital · JPUniversity of Occupational and Environmental Health Japan · JP

Funding

Japan Society for the Promotion of Science 16H05162Japan Society for the Promotion of Science 16K09247Japan Society for the Promotion of Science 16K15503Japan Society for the Promotion of Science 20H03459
6 · The paper itself

Abstract

Cholesterol is an essential plasma membrane lipid for the maintenance of cellular homeostasis and cancer cell proliferation. Free cholesterol is harmful to cells; therefore, excessive free cholesterol must be quickly esterified by acetyl-coenzyme A:cholesterol acetyltransferase (ACAT) and exported by scavenger receptor class B member I (SR-BI) or ATP-binding cassette protein A1 from specific cells such as macrophage foam cells, which contain cholesteryl ester-derived vacuoles. Many vacuoles are present in the cytoplasm of Burkitt lymphoma cells. In this study, we observed that these vacuoles are often seen in high-grade lymphomas. Cell culture study using lymphoma cell lines found that esterified cholesterol is the main component of these vacuoles and the expression of cholesterol metabolism-related molecules was significantly upregulated in lymphoma cell lines, with SR-BI and ACAT inhibitors (BLT-1 and CI-976, respectively) impeding lymphoma cell proliferation. Cytoplasmic free cholesterol was increased by ACAT and SR-BI inhibitors, and the accumulation of free cholesterol induced lymphoma cell apoptosis by inducing endoplasmic reticulum stress. Furthermore, synergistic effects of SR-BI and ACAT inhibitors were observed in a preclinical study. Treatment with SR-BI inhibitor suppressed lymphoma progression in a tumor-bearing mouse model, whereas ACAT inhibitor did not. Therefore, SR-BI inhibitors are potential new antilymphoma therapeutics that target cholesterol metabolism.

Indexed as

ATP-Binding Cassette TransportersFoam CellsAnimalsCholesterolCholesterol EstersHumansMiceScavenger Receptors, Class BATP-Binding Cassette TransportersCholesterolCholesterol EstersScavenger Receptors, Class BACATcholesterolER stresslymphomaSR-BI

Identifiers

PMID35343027
PMCPMC9207360
OpenAlexW4220763766

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.