Evidence map›Paper›PMID 35806209›Full record

ReviewInternational journal of molecular sciences2022

Linking Late Endosomal Cholesterol with Cancer Progression and Anticancer Drug Resistance.

Mai K L Nguyen, Jaimy Jose, Mohamed Wahba, Marc Bernaus-Esqué, Andrew J Hoy, Carlos Enrich, Carles Rentero, Thomas Grewal

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.7field-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

26 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Organelle contact sites in cancer cells.Cell death & disease · 2026
    Review
  3. Article
  4. Review
  5. The emerging role of cholesterol metabolism in gynecologic cancer development and therapy.Apoptosis : an international journal on programmed cell death · 2026
    Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Dysregulation of cholesterol homeostasis in cancer pathogenesis.Cellular and molecular life sciences : CMLS · 2025
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Review
  20. 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

8 authors at 2 institutions in 2 countries.

Mai K L NguyenSchool of Pharmacy, Faculty of Medicine and Health, University of Sydney, Sydney, NSW 2006, Australia.
Jaimy JoseSchool of Pharmacy, Faculty of Medicine and Health, University of Sydney, Sydney, NSW 2006, Australia.
Mohamed WahbaSchool of Pharmacy, Faculty of Medicine and Health, University of Sydney, Sydney, NSW 2006, Australia.
Marc Bernaus-EsquéDepartament de Biomedicina, Unitat de Biologia Cel·lular, Facultat de Medicina i Ciències de la Salut, Universitat de Barcelona, 08036 Barcelona, Spain.ORCID 0000-0002-8200-6291
Andrew J HoySchool of Medical Sciences, Charles Perkins Centre, Faculty of Medicine and Health, University of Sydney, Sydney, NSW 2006, Australia.ORCID 0000-0003-3922-1137
Carlos EnrichDepartament de Biomedicina, Unitat de Biologia Cel·lular, Facultat de Medicina i Ciències de la Salut, Universitat de Barcelona, 08036 Barcelona, Spain.ORCID 0000-0003-0382-2993
Carles RenteroDepartament de Biomedicina, Unitat de Biologia Cel·lular, Facultat de Medicina i Ciències de la Salut, Universitat de Barcelona, 08036 Barcelona, Spain.ORCID 0000-0003-4684-0278
Thomas GrewalSchool of Pharmacy, Faculty of Medicine and Health, University of Sydney, Sydney, NSW 2006, Australia.ORCID 0000-0002-7937-8887
The University of Sydney · AUDepartament de Salut · ES

Funding

Government of Catalonia Serra Húnter ProgrammeMinisterio de Ciencia e Innovación PID2020-115910RB-I00University of Sydney RY859
6 · The paper itself

Abstract

Cancer cells undergo drastic metabolic adaptions to cover increased bioenergetic needs, contributing to resistance to therapies. This includes a higher demand for cholesterol, which often coincides with elevated cholesterol uptake from low-density lipoproteins (LDL) and overexpression of the LDL receptor in many cancers. This implies the need for cancer cells to accommodate an increased delivery of LDL along the endocytic pathway to late endosomes/lysosomes (LE/Lys), providing a rapid and effective distribution of LDL-derived cholesterol from LE/Lys to other organelles for cholesterol to foster cancer growth and spread. LDL-cholesterol exported from LE/Lys is facilitated by Niemann-Pick Type C1/2 (NPC1/2) proteins, members of the steroidogenic acute regulatory-related lipid transfer domain (StARD) and oxysterol-binding protein (OSBP) families. In addition, lysosomal membrane proteins, small Rab GTPases as well as scaffolding proteins, including annexin A6 (AnxA6), contribute to regulating cholesterol egress from LE/Lys. Here, we summarize current knowledge that links upregulated activity and expression of cholesterol transporters and related proteins in LE/Lys with cancer growth, progression and treatment outcomes. Several mechanisms on how cellular distribution of LDL-derived cholesterol from LE/Lys influences cancer cell behavior are reviewed, some of those providing opportunities for treatment strategies to reduce cancer progression and anticancer drug resistance.

Indexed as

Antineoplastic AgentsNeoplasmsCholesterolCholesterol, LDLEndosomesHumansLysosomesNiemann-Pick C1 Proteinrab GTP-Binding ProteinsAntineoplastic AgentsCholesterolCholesterol, LDLNiemann-Pick C1 Proteinrab GTP-Binding ProteinsAnnexin A6cancercholesterol transporterslate endosomes/lysosomesLDL-cholesterolNPC1Rab7StARD3

Identifiers

PMID35806209
PMCPMC9267071
OpenAlexW4283713416

What Socratic 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 Socratic graph.