ReviewWorld journal of gastroenterology2017
Relation of the IGF/IGF1R system to autophagy in colitis and colorectal cancer.
Review in World journal of gastroenterology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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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.
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.
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Who cites it
13 citing papers in PubMed, 29 citations in OpenAlex.
- A bioinformatics analysis of the target role of miRNA-431-5p on KLK6 in colorectal cancer.Hereditas · 2025Article
- Exploring the potential regulation of DUOX in thyroid hormone‑autophagy signaling via IGF‑1 in the skeletal muscle (Review).Biomedical reports · 2025Review
- Association of "a body shape index" with the risk of developing colorectal cancer in U.S. patients with metabolic syndrome: evidence from the NHANES 1999-2018.BMC gastroenterology · 2024Article
- Sirtuins Affect Cancer Stem Cells via Epigenetic Regulation of Autophagy.Biomedicines · 2024Review
- The role of imprinting genes' loss of imprints in cancers and their clinical implications.Frontiers in oncology · 2024Review
- Autophagy and the Insulin-like Growth Factor (IGF) System in Colonic Cells: Implications for Colorectal Neoplasia.International journal of molecular sciences · 2023Review
- Survival of HT29 Cancer Cells Is Affected by IGF1R InhibitionPathology oncology research : POR · 2022Article
- Mild hyperthermia induced by gold nanorods acts as a dual-edge blade in the fate of SH-SY5Y cells via autophagy.Scientific reports · 2021Article
- Growth Factors, PI3K/AKT/mTOR and MAPK Signaling Pathways in Colorectal Cancer Pathogenesis: Where Are We Now?International journal of molecular sciences · 2021Review
- Baicalein Ameliorates Epilepsy Symptoms in a Pilocarpine-Induced Rat Model by Regulation of IGF1R.Neurochemical research · 2020Article
- IGF2 loss of imprinting enhances colorectal cancer stem cells pluripotency by promoting tumor autophagy.Aging · 2020Article
- Review
- Oral Administration of MicroencapsulatedInternational journal of molecular sciences · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metabolic syndrome (MetS), as a chronic inflammatory disorder has a potential role in the development of inflammatory and cancerous complications of the colonic tissue. The interaction of DNA damage and inflammation is affected by the insulin-like growth factor 1 receptor (IGF1R) signaling pathway. The IGF1R pathway has been reported to regulate autophagy, as well, but sometimes through a bidirectional context. Targeting the IGF1R-autophagy crosstalk could represent a promising strategy for the development of new antiinflammatory and anticancer therapies, and may help for subjects suffering from MetS who are at increased risk of colorectal cancer. However, therapeutic responses to targeted therapies are often shortlived, since a signaling crosstalk of IGF1R with other receptor tyrosine kinases or autophagy exists, leading to acquired cellular resistance to therapy. From a pharmacological point of view, it is attractive to speculate that synergistic benefits could be achieved by inhibition of one of the key effectors of the IGF1R pathway, in parallel with the pharmacological stimulation of the autophagy machinery, but cautiousness is also required, because pharmacologic IGF1R modulation can initiate additional, sometimes unfavorable biologic effects.
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What OpenQuestion holds
Registered trials
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.