ArticleInternational journal of molecular sciences2017
AA-NAT, MT1 and MT2 Correlates with Cancer Stem-Like Cell Markers in Colorectal Cancer: Study of the Influence of Stage and p53 Status of Tumors.
Article in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Regulation of Stemness by NR1D2 in Colorectal Cancer.Biomedicines · 2025Article
- iNOS-Produced Nitric Oxide from Cancer Cells as an Intermediate of Stemness Regulation by PARP-1 in Colorectal Cancer.Biomolecules · 2025Article
- Resveratrol and p53: How are they involved in CRC plasticity and apoptosis?Journal of advanced research · 2024Review
- Agomelatine, a Melatonin-Derived Drug, as a New Strategy for the Treatment of Colorectal Cancer.Antioxidants (Basel, Switzerland) · 2023Article
- PARP-1 Expression Influences Cancer Stem Cell Phenotype in Colorectal Cancer Depending on p53.International journal of molecular sciences · 2023Article
- CD166-specific CAR-T cells potently target colorectal cancer cells.Translational oncology · 2023Article
- Article
- Endothelin-1 as a Mediator of Heme Oxygenase-1-Induced Stemness in Colorectal Cancer: Influence of p53.Journal of personalized medicine · 2021Article
- Glioblastoma chemoresistance: roles of the mitochondrial melatonergic pathway.Cancer drug resistance (Alhambra, Calif.) · 2020Review
- Circadian Genes as Therapeutic Targets in Pancreatic Cancer.Frontiers in endocrinology · 2020Review
- Melatonin is a potential inhibitor of ovarian cancer: molecular aspects.Journal of ovarian research · 2019Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The characterization of colon cancer stem cells (CSCs) may help to develop novel diagnostic and therapeutic procedures. p53 loss increases the pool of CSCs in colorectal cancer (CRC). Recent reports suggest that the oncostatic effects of melatonin could be related to its ability to kill CSCs. Although there are no data linking the loss of p53 function and melatonin synthesis or signaling in cancer, melatonin does activate the p53 tumor-suppressor pathway in this disease. In this work, we analyze whether the expression of melatonin synthesis and signaling genes are related to the expression of CSC markers and the implication of p53 status in samples from patients with CRC. Arylalkylamine N-acetyltransferase (AA-NAT), MT1, and MT2 expression decreased in tumor samples versus normal mucosa samples in mutated p53 (mtp53) tumors versus those with wild-type p53 (wtp53). Further, AA-NAT and MT2 expression were lower in advanced stages of the disease in wtp53 tumors. On the contrary, CD44 and CD66c expression was higher in tumor versus normal mucosa in wtp53 tumors. Additionally, CD44 expression was higher in advanced stages of the disease regardless of the p53 status. Patients with CD44
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