Evidence map›Paper›PMID 27455418›Full record

ArticleCancer biology & therapy2016

Methylglyoxal suppresses human colon cancer cell lines and tumor growth in a mouse model by impairing glycolytic metabolism of cancer cells associated with down-regulation of c-Myc expression.

Tiantian He, Huaibin Zhou, Chunmei Li, Yuan Chen, Xiaowan Chen, Chenli Li, Jiating Mao, Jianxin Lyu, Qing H Meng

Open access · bronzeAbstract read
In one paragraph

Article in Cancer biology & therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Methylglyoxal AttenuatesInternational journal of molecular sciences · 2026
    Article
  3. Article
  4. Frontiers in veterinary science · 2025
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. 29th Annual GP2A Medicinal Chemistry Conference.Pharmaceuticals (Basel, Switzerland) · 2021
    Article
  10. Article
  11. Review
  12. Article
  13. EXCLI journal · 2020
    Article
  14. Article
  15. Article
  16. 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

9 authors at 2 institutions in 2 countries.

Tiantian Hea Key Laboratory of Laboratory Medicine , Ministry of Education of China, Zhejiang Provincial Key Laboratory of Medical Genetics, School of Laboratory Medicine and Life Sciences, Wenzhou Medical University , Wenzhou, Zhejiang , China.
Huaibin Zhoua Key Laboratory of Laboratory Medicine , Ministry of Education of China, Zhejiang Provincial Key Laboratory of Medical Genetics, School of Laboratory Medicine and Life Sciences, Wenzhou Medical University , Wenzhou, Zhejiang , China.
Chunmei Lia Key Laboratory of Laboratory Medicine , Ministry of Education of China, Zhejiang Provincial Key Laboratory of Medical Genetics, School of Laboratory Medicine and Life Sciences, Wenzhou Medical University , Wenzhou, Zhejiang , China.
Yuan Chena Key Laboratory of Laboratory Medicine , Ministry of Education of China, Zhejiang Provincial Key Laboratory of Medical Genetics, School of Laboratory Medicine and Life Sciences, Wenzhou Medical University , Wenzhou, Zhejiang , China.
Xiaowan Chena Key Laboratory of Laboratory Medicine , Ministry of Education of China, Zhejiang Provincial Key Laboratory of Medical Genetics, School of Laboratory Medicine and Life Sciences, Wenzhou Medical University , Wenzhou, Zhejiang , China.
Chenli Lia Key Laboratory of Laboratory Medicine , Ministry of Education of China, Zhejiang Provincial Key Laboratory of Medical Genetics, School of Laboratory Medicine and Life Sciences, Wenzhou Medical University , Wenzhou, Zhejiang , China.
Jiating Maoa Key Laboratory of Laboratory Medicine , Ministry of Education of China, Zhejiang Provincial Key Laboratory of Medical Genetics, School of Laboratory Medicine and Life Sciences, Wenzhou Medical University , Wenzhou, Zhejiang , China.
Jianxin Lyua Key Laboratory of Laboratory Medicine , Ministry of Education of China, Zhejiang Provincial Key Laboratory of Medical Genetics, School of Laboratory Medicine and Life Sciences, Wenzhou Medical University , Wenzhou, Zhejiang , China.
Qing H Mengb Department of Laboratory Medicine , The University of Texas MD Anderson Cancer Center , Houston , TX , USA.
Wenzhou Medical University · CNThe University of Texas MD Anderson Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Methylglyoxal (MG) is a highly reactive dicarbonyl compound exhibiting anti-tumor activity. The anti-tumor effects of MG have been demonstrated in some types of cancer, but its role in colon cancer and the mechanisms underlying this activity remain largely unknown. We investigated its role in human colon cancer and the underlying mechanism using human colon cancer cells and animal model. Viability, proliferation, and apoptosis were quantified in DLD-1 and SW480 colon cancer cells by using the Cell Counting Kit-8, plate colony formation assay, and flow cytometry, respectively. Cell migration and invasion were assessed by wound healing and transwell assays. Glucose consumption, lactate production, and intracellular ATP production also were assayed. The levels of c-Myc protein and mRNA were quantitated by western blot and qRT-PCR. The anti-tumor role of MG in vivo was investigated in a DLD-1 xenograft tumor model in nude mice. We demonstrated that MG inhibited viability, proliferation, migration, and invasion and induced apoptosis of DLD-1 and SW480 colon cancer cells. Treatment with MG reduced glucose consumption, lactate production, and ATP production and decreased c-Myc protein levels in these cells. Moreover, MG significantly suppressed tumor growth and c-Myc expression in vivo. Our findings suggest that MG plays an anti-tumor role in colon cancer. It inhibits cancer cell growth by altering the glycolytic pathway associated with downregulation of c-Myc protein. MG has therapeutic potential in colon cancer by interrupting cancer metabolism.

Indexed as

AnimalsCell Line, TumorColonic NeoplasmsDisease Models, AnimalDown-RegulationGlycolysisHumansMiceMice, NudeProto-Oncogene Proteins c-mycPyruvaldehydeProto-Oncogene Proteins c-mycPyruvaldehydeAnti-tumorc-Myccolon cancerglycolysismethylglyoxal

Identifiers

PMID27455418
PMCPMC5036412
OpenAlexW2476318571

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.