Evidence map›Paper›PMID 40430358›Full record

ArticleMolecules (Basel, Switzerland)2025

Colchicine Binding Site Tubulin Inhibitors Impair Vincristine-Resistant Neuroblastoma Cell Function.

Cinthia N Reed, Kaylee B Garrison, Joshua Thammathong, Jindrich Cinatl, Martin Michaelis, Souvik Banerjee, April M Weissmiller

Abstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Flavonoids as colchicine binding site inhibitors: emerging scaffolds in anticancer drug design.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2026
    Review
  2. 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

7 authors.

Cinthia N ReedDepartment of Biology, Middle Tennessee State University, Murfreesboro, TN 37132, USA.
Kaylee B GarrisonDepartment of Biology, Middle Tennessee State University, Murfreesboro, TN 37132, USA.
Joshua ThammathongDepartment of Chemistry, Middle Tennessee State University, Murfreesboro, TN 37132, USA.
Jindrich CinatlDr Petra Joh Research Institute, Frankfurter Stiftung für Krebskranke Kinder, 60528 Frankfurt am Main, Germany.ORCID 0000-0002-6744-2087
Martin MichaelisDr Petra Joh Research Institute, Frankfurter Stiftung für Krebskranke Kinder, 60528 Frankfurt am Main, Germany.ORCID 0000-0002-5710-5888
Souvik BanerjeeDepartment of Chemistry, Middle Tennessee State University, Murfreesboro, TN 37132, USA.ORCID 0000-0002-7811-2577
April M WeissmillerDepartment of Biology, Middle Tennessee State University, Murfreesboro, TN 37132, USA.ORCID 0000-0003-4505-0530

Funding

Determining the significance of the N-MYC-WDR5 interaction in neuroblastoma.R15CA263868 · NCI · MIDDLE TENNESSEE STATE UNIVERSITY · PI WEISSMILLER, APRIL M. · 2021 to 2021
$380k
NCI NIH HHS R15 CA263868NIH HHS 1R16GM154786-25A1NIH/NCI CA263868
6 · The paper itself

Abstract

High-risk neuroblastoma remains a clinically challenging pediatric cancer, with an approximate five-year survival rate of ~60%. Frontline therapy for this group of patients includes surgery and intensive chemotherapy that involves combinations of the tubulin inhibitor vincristine with several other chemotherapeutics. Unfortunately, unresponsiveness to therapy and relapse are common, with tumors often displaying resistance to vincristine. Recently, we characterized a novel set of tubulin inhibitors that are distinct from vincristine and bind within the colchicine binding site present on tubulin monomers. Colchicine binding site inhibitors (CBSIs) have gained traction as improved chemotherapeutics due to their potential to overcome tubulin inhibitor-induced resistance. In this study, we investigate the functional impact of CBSI treatment on multiple neuroblastoma cell lines, including those that are vincristine-resistant. We demonstrate that our newly developed compounds are effective at disrupting cell division in non-resistant and resistant cells and have cellular activity against vincristine-resistant cell lines. Interestingly, we find that vincristine-resistant cell lines differ in their ability to undergo apoptotic cell death in response to CBSI treatment. Taken together, these findings provide a solid foundation to further investigate the utility of CBSIs for neuroblastoma treatment, while highlighting the distinct resistance mechanisms that can emerge in these childhood cancers.

Indexed as

ColchicineDrug Resistance, NeoplasmNeuroblastomaTubulinTubulin ModulatorsVincristineApoptosisBinding SitesCell Line, TumorCell ProliferationHumansColchicineTubulinTubulin ModulatorsVincristineALKcolchicine binding site inhibitorMYCNneuroblastomatubulinvincristine

Identifiers

PMID40430358
PMCPMC12113804

What OpenQuestion holds

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Registered trials

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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.