Evidence map›Paper›PMID 24466327›Full record

ArticlePloS one2014

Novel analogue of colchicine induces selective pro-death autophagy and necrosis in human cancer cells.

Kristen Larocque, Pamela Ovadje, Sinisa Djurdjevic, Mariam Mehdi, James Green, Siyaram Pandey

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. 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
6.4field-weighted citation impact, top 3% 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, 70 citations in OpenAlex.

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  5. Doxorubicin-induced chemoresistance in Duke's type B colon adenocarcinoma cell line is aggravated in the presence of TGF-β2 through non-apoptotic cell death.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024
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  14. Mitotic Poisons in Research and Medicine.Molecules (Basel, Switzerland) · 2020
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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.

Kristen LarocqueDepartment of Chemistry & Biochemistry, University of Windsor, Windsor, Onatrio, Canada.
Pamela OvadjeDepartment of Chemistry & Biochemistry, University of Windsor, Windsor, Onatrio, Canada.
Sinisa DjurdjevicDepartment of Chemistry & Biochemistry, University of Windsor, Windsor, Onatrio, Canada.
Mariam MehdiDepartment of Chemistry & Biochemistry, University of Windsor, Windsor, Onatrio, Canada.
James GreenDepartment of Chemistry & Biochemistry, University of Windsor, Windsor, Onatrio, Canada.
Siyaram PandeyDepartment of Chemistry & Biochemistry, University of Windsor, Windsor, Onatrio, Canada.
University of Windsor · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colchicine, a natural product of Colchicum autumnae currently used for gout treatment, is a tubulin targeting compound which inhibits microtubule formation by targeting fast dividing cells. This tubulin-targeting property has lead researchers to investigate the potential of colchicine and analogs as possible cancer therapies. One major study conducted on an analogue of allocolchicine, ZD 6126, was halted in phase 2 clinical trials due to severe cardio-toxicity associated with treatment. This study involves the development and testing of novel allocolchicine analogues that hold non-toxic anti-cancer properties. Currently we have synthesized and evaluated the anti-cancer activities of two analogues; N-acetyl-O-methylcolchinol (NSC 51046 or NCME), which is structurally similar to ZD 6126, and (S)-3,8,9,10-tetramethoxyallocolchicine (Green 1), which is a novel derivative of allocolchicine that is isomeric in the A ring. NSC 51046 was found to be non-selective as it induced apoptosis in both BxPC-3 and PANC-1 pancreatic cancer cells and in normal human fibroblasts. Interestingly, we found that Green 1 was able to modestly induce pro-death autophagy in these pancreatic cancer cells and E6-1 leukemia cells but not in normal human fibroblasts. Unlike colchicine and NSC 51046, Green 1 does not appear to affect tubulin polymerization indicating that it has a different molecular target. Green 1 also caused increased reactive oxygen species (ROS) production in mitochondria isolated from pancreatic cancer cells. Furthermore, in vivo studies revealed that Green 1 was well tolerated in mice. Our findings suggest that a small change in the structure of colchicine has apparently changed the mechanism of action and lead to improved selectivity. This may lead to better selective treatments in cancer therapy.

Indexed as

NecrosisAnimalsAntineoplastic AgentsAutophagyBlotting, WesternCell ProliferationCells, CulturedColchicineFibroblastsHumansLeukemia, T-CellMaleMiceMice, NudeMicrotubulesMitochondria3,8,9,10-tetramethoxyallocolchicineallocolchicineAntineoplastic AgentsColchicineNSC 51046Reactive Oxygen SpeciesTubulin

Identifiers

PMID24466327
PMCPMC3900699
OpenAlexW1984406525

What OpenQuestion holds

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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.