Evidence map›Paper›PMID 28805013›Full record

ArticleMacromolecular bioscience2018

Drug-Free Macromolecular Therapeutics Induce Apoptosis via Calcium Influx and Mitochondrial Signaling Pathway.

Lian Li, Jiyuan Yang, Jiawei Wang, Jindřich Kopeček

Open access · greenAbstract read
In one paragraph

Article in Macromolecular bioscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

25 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Multi-targeted immunotherapeutics to treat B cell malignancies.Journal of controlled release : official journal of the Controlled Release Society · 2023
    Review
  9. Article
  10. Review
  11. Review
  12. Ginsenoside Rk1 protects human melanocytes from HMolecular medicine reports · 2021
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Polymer nanomedicines.Advanced drug delivery reviews · 2020
    Review
  18. Article
  19. Article
  20. Overcoming chemotherapy resistanceActa pharmaceutica Sinica. B · 2019
    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

4 authors at 1 institution in 1 country.

Lian LiDepartment of Pharmaceutics and Pharmaceutical Chemistry/CCCD, University of Utah, Salt Lake City, UT, 84112, USA.
Jiyuan YangDepartment of Pharmaceutics and Pharmaceutical Chemistry/CCCD, University of Utah, Salt Lake City, UT, 84112, USA.
Jiawei WangDepartment of Pharmaceutics and Pharmaceutical Chemistry/CCCD, University of Utah, Salt Lake City, UT, 84112, USA.
Jindřich KopečekDepartment of Pharmaceutics and Pharmaceutical Chemistry/CCCD, University of Utah, Salt Lake City, UT, 84112, USA.
University of Utah · US

Funding

Drug-Free Macromolecular TherapeuticsR01GM095606 · NIGMS · UNIVERSITY OF UTAH · PI KOPECEK, JINDRICH H. · 2011 to 2018
$2.3M
NIGMS NIH HHS R01 GM095606
6 · The paper itself

Abstract

Recently, an innovative paradigm has been proposed in macromolecular therapeutics for treatment of B-cell lymphomas that can specifically kill cancer cells without a drug. The design rationale of this drug-free macromolecular therapeutic (DFMT) system is crosslinking the cell surface receptor to initiate apoptosis. However, how the apoptosis signal is triggered after receptor hyper-crosslinking remains to be elucidated. Here, two pathways, calcium influx dependent pathway and mitochondrial signal pathway, are identified to play major roles in triggering the programmed cell death. With the first step pretargeting and second step multiple binding, receptor hyper-crosslinking is achieved in a highly specific, time-dependent manner and largely mediated by multivalence. As a consequence, extracellular calcium influx is triggered, which subsequently decreases the mitochondrial membrane potential and induces apoptosis. The mitochondrial depolarization also stems from the Bcl-2 inhibition mediated by DFMT, followed by the cytochrome c release that activates caspase signaling. With the participation of the two-pronged mechanism, a programmed apoptosis is induced in response to DFMT treatment. The current findings can offer important implications to optimize the anti-CD20 strategies to treat B-cell non-Hodgkin lymphomas.

Indexed as

Molecular Targeted TherapyAntigens, CD20ApoptosisCalciumCaspasesCytochromes cHumansLymphoma, B-CellMembrane Potential, MitochondrialMitochondriaProto-Oncogene Proteins c-bcl-2Signal TransductionAntigens, CD20CalciumCaspasesCytochromes cProto-Oncogene Proteins c-bcl-2apoptosiscancer therapydrug-free macromolecular therapeuticslymphomareceptor crosslinking

Identifiers

PMID28805013
PMCPMC5912161
OpenAlexW2748955709

What OpenQuestion holds

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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.