Evidence map›Paper›PMID 34371753›Full record

ReviewPharmaceutics2021

Behind the Adaptive and Resistance Mechanisms of Cancer Stem Cells to TRAIL.

Adriana G Quiroz-Reyes, Paulina Delgado-Gonzalez, Jose Francisco Islas, Juan Luis Delgado Gallegos, Javier Humberto Martínez Garza, Elsa N Garza-Treviño

Open access · goldAbstract readReview
In one paragraph

Review in Pharmaceutics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

12 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Small molecule activators of TAK1 promotes its activity-dependent ubiquitination and TRAIL-mediated tumor cell death.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  7. Cell Therapy as Target Therapy against Colon Cancer Stem Cells.International journal of molecular sciences · 2023
    Review
  8. Novel Anticancer Strategies II.Pharmaceutics · 2023
    Article
  9. Article
  10. Review
  11. Review
  12. The role of histone deacetylase 3 in breast cancer.Medical oncology (Northwood, London, England) · 2022
    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

6 authors at 1 institution in 1 country.

Adriana G Quiroz-ReyesDepartment of Biochemistry and Molecular Medicine, Faculty of Medicine, Autonomous University of Nuevo Leon, San Nicolás de los Garza 64460, Mexico.
Paulina Delgado-GonzalezDepartment of Biochemistry and Molecular Medicine, Faculty of Medicine, Autonomous University of Nuevo Leon, San Nicolás de los Garza 64460, Mexico.
Jose Francisco IslasDepartment of Biochemistry and Molecular Medicine, Faculty of Medicine, Autonomous University of Nuevo Leon, San Nicolás de los Garza 64460, Mexico.ORCID 0000-0002-0337-9912
Juan Luis Delgado GallegosDepartment of Biochemistry and Molecular Medicine, Faculty of Medicine, Autonomous University of Nuevo Leon, San Nicolás de los Garza 64460, Mexico.ORCID 0000-0003-1580-0812
Javier Humberto Martínez GarzaDepartment of Human Anatomy, Faculty of Medicine, Autonomous University of Nuevo Leon, San Nicolás de los Garza 64460, Mexico.
Elsa N Garza-TreviñoDepartment of Biochemistry and Molecular Medicine, Faculty of Medicine, Autonomous University of Nuevo Leon, San Nicolás de los Garza 64460, Mexico.
Universidad Autónoma de Nuevo León · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL), also known as Apo-2 ligand (Apo2L), is a member of the TNF cytokine superfamily. TRAIL has been widely studied as a novel strategy for tumor elimination, as cancer cells overexpress TRAIL death receptors, inducing apoptosis and inhibiting blood vessel formation. However, cancer stem cells (CSCs), which are the main culprits responsible for therapy resistance and cancer remission, can easily develop evasion mechanisms for TRAIL apoptosis. By further modifying their properties, they take advantage of this molecule to improve survival and angiogenesis. The molecular mechanisms that CSCs use for TRAIL resistance and angiogenesis development are not well elucidated. Recent research has shown that proteins and transcription factors from the cell cycle, survival, and invasion pathways are involved. This review summarizes the main mechanism of cell adaption by TRAIL to promote response angiogenic or pro-angiogenic intermediates that facilitate TRAIL resistance regulation and cancer progression by CSCs and novel strategies to induce apoptosis.

Indexed as

angiogenesiscancer stem cellsTRAILTRAIL resistance

Identifiers

PMID34371753
PMCPMC8309156
OpenAlexW3179692090

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.