Evidence map›Paper›PMID 26239968›Full record

ArticleJournal of neuro-oncology2015

Colchicine derivative as a potential anti-glioma compound.

Kuan-Min Fang, Jun-Jen Liu, Chun-Chun Li, Chih-Chi Cheng, Yun-Ti Hsieh, Kit Man Chai, Yu-An Lien, Shun-Fen Tzeng

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of neuro-oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

7 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. 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 1 country.

Kuan-Min FangDepartment of Life Sciences, College of Bioscience and Biotechnology, National Cheng Kung University, Tainan, Taiwan, ROC.
Jun-Jen LiuSchool of Medical Laboratory Science and Biotechnology, Taipei Medical University, Taipei, Taiwan, ROC.
Chun-Chun LiDepartment of Life Sciences, College of Bioscience and Biotechnology, National Cheng Kung University, Tainan, Taiwan, ROC.
Chih-Chi ChengDepartment of Life Sciences, College of Bioscience and Biotechnology, National Cheng Kung University, Tainan, Taiwan, ROC.
Yun-Ti HsiehDepartment of Life Sciences, College of Bioscience and Biotechnology, National Cheng Kung University, Tainan, Taiwan, ROC.
Kit Man ChaiDepartment of Life Sciences, College of Bioscience and Biotechnology, National Cheng Kung University, Tainan, Taiwan, ROC.
Yu-An LienDepartment of Life Sciences, College of Bioscience and Biotechnology, National Cheng Kung University, Tainan, Taiwan, ROC.
Shun-Fen TzengDepartment of Life Sciences, College of Bioscience and Biotechnology, National Cheng Kung University, Tainan, Taiwan, ROC. stzeng@mail.ncku.edu.tw.
National Cheng Kung University · TWTaipei Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colchicine, an anti-microtubule and antimitotic drug, is a common therapeutically agent for gout, which is thought to have potential anti-tumor effects. Owing to concerns of colchicines poisoning, the development of derivatives with low dose efficacy and less side effects is of obvious interest. In this study, we characterized the inhibitory effects of a colchicine derivative named AD1 on the cell proliferation of human malignant glioblastoma (MG) cell lines, U87MG and U373MG. We found that 50 % of U87MG and U373MG cells were reduced in the cultures after exposure to AD1 for 24 h at 10 and 50 nM, respectively. Moreover, α-tubulin immunostaining indicated that AD1 induced the disruption of the microtubule polymerization in glioma cells with apoptotic features including membrane budding/blebbing or fragmented nuclei. Increased levels of reactive oxygen species (ROS) were also detected in AD1-treated U87MG and U373MG cells compared to that observed in the control culture. Moreover, examination of microtubule-associated protein 1A/1B-light chain 3 (LC3I)/LC3II conversion and acridine orange staining for autophagic vesicles, combined with flow cytometry, showed that treatment with AD1 induced the autophagic pathway in U87MG and U373MG cells. Furthermore, we found that the intermittent intravenous administration of AD1 suppressed glioma growth in rat brain receiving intracerebral injection with rat C6 glioma cells. Taken together, our findings reveal that treatment with AD1 at nanomolar scales can reduce glioma cell viability effectively, with the occurrence of a rise in ROS and cellular autophagy. In conjunction with the observations from in vivo study, the colchicine derivative AD1 has chemotherapeutic potential to suppress glioma progression.

Indexed as

AnimalsAntineoplastic AgentsAutophagyBrain NeoplasmsCell Line, TumorCell SurvivalColchicineDisease Models, AnimalDose-Response Relationship, DrugFemaleGlioblastomaHumansOxidative StressRatsRats, Sprague-DawleyReactive Oxygen SpeciesAntineoplastic AgentsColchicineReactive Oxygen SpeciesTubulinAcidic vesicular organellesAD1AutophagyColchicineGlioma

Identifiers

PMID26239968
OpenAlexW1101779487

What OpenQuestion holds

Textmetadata
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.