ArticleWorld journal of gastrointestinal oncology2014
Growth inhibition of colon cancer cells by compounds affecting AMPK activity.
Article in World journal of gastrointestinal oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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13 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- Will metformin use lead to a decreased risk of thyroid cancer? A systematic review and meta-analyses.European journal of medical research · 2023Pooled it
- Phenformin suppresses angiogenesis through the regulation of exosomal microRNA-1246 and microRNA-205 levels derived from oral squamous cell carcinoma cells.Frontiers in oncology · 2022Article
- Long Non-Coding RNA and mRNA Expression Analysis in Liver of Mice WithFrontiers in cellular and infection microbiology · 2021Article
- Metformin alleviates breast cancer through targeting high-mobility group AT-hook 2.Thoracic cancer · 2020Article
- Effects of metformin and phenformin on apoptosis and epithelial-mesenchymal transition in chemoresistant rectal cancer.Cancer science · 2019Article
- Advances in the Antagonism of Epigallocatechin-3-gallate in the Treatment of Digestive Tract Tumors.Molecules (Basel, Switzerland) · 2019Review
- Anticancer effects of resveratrol in canine hemangiosarcoma cell lines.Veterinary and comparative oncology · 2018Article
- Synergistic cytotoxicity of the dipeptidyl peptidase-IV inhibitor gemigliptin with metformin in thyroid carcinoma cells.Endocrine · 2018Article
- Gomisin A Suppresses Colorectal Lung Metastasis by Inducing AMPK/p38-Mediated Apoptosis and Decreasing Metastatic Abilities of Colorectal Cancer Cells.Frontiers in pharmacology · 2018Article
- Effects of Resveratrol, Lovastatin and the mTOR-Inhibitor RAD-001 on Insulin-Induced Genomic Damage In Vitro.Molecules (Basel, Switzerland) · 2017Article
- Metformin inhibits thyroid cancer cell growth, migration, and EMT through the mTOR pathway.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- Dissecting the Dual Role of AMPK in Cancer: From Experimental to Human Studies.Molecular cancer research : MCR · 2015Review
- Network-Based Analysis of Nutraceuticals in Human Hepatocellular Carcinomas Reveals Mechanisms of Chemopreventive Action.CPT: pharmacometrics & systems pharmacology · 2015Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo determine if other molecules reported to modulate AMP-dependent protein kinase (AMPK) activity would have effects resembling those of metformin and phenformin on colon cancer cell proliferation and metabolism.
methodsStudies were performed with four human colon cancer cell lines, Caco-2, HCT116, HT29 and SW1116. The compounds that were studied included A-769662, 5-aminoimidazole-4-carboxamide-1-ribofuranoside, butyrate, (-)-epigallocatechin gallate (EGCG), KU-55933, quercetin, resveratrol and salicylates. The parameters that were measured were cell proliferation and viability, glucose uptake, lactate production and acidification of the incubation medium.
resultsInvestigations with several molecules that have been reported to be associated with AMPK activation (A-769662, 5-aminoimidazole-4-carboxamide-1-b-D-ribofuranoside, EGCG, KU-55933, quercetin, resveratrol and salicylates) or AMPK inhibition (compound C) failed to reveal increased medium acidification and increased glucose uptake in colon cancer cells as previously established with metformin and phenformin. The only exception was 5-aminosalicylic acid with which there were apparently lower glucose levels in the medium after incubation for 72 h. Further study in the absence of cells revealed that the effect was an artifact due to inhibition of the enzyme-linked glucose assay. The compounds were studied at concentrations that inhibited cell proliferation.
conclusionIt was concluded that treatment with several agents that can affect AMPK activity resulted in the inhibition of the proliferation of colon cancer cells under conditions in which glucose metabolism is not enhanced, in contrast to the effect of biguanides.
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