ArticleInternational journal of oncology2014
Preoperative low dose NSAID treatment influences the genes for stemness, growth, invasion and metastasis in colorectal cancer.
Article in International journal of oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 22 citations in OpenAlex.
- Celecoxib-Induced Modulation of Colon Cancer CD133 Expression Occurs through AKT Inhibition and Is Monitored byMolecular imaging · 2022Article
- Modified Systemic Inflammation Score Is an Independent Predictor of Long-Term Outcome in Patients Undergoing Surgery for Adenocarcinoma of the Esophagogastric Junction.Frontiers in surgery · 2021Article
- A Novel Inflammatory-Nutritional Prognostic Scoring System for Stage III Gastric Cancer Patients With Radical Gastrectomy Followed by Adjuvant Chemotherapy.Frontiers in oncology · 2021Article
- Role of Anti-inflammatory Drugs in the Colorectal Cancer.Hospital pharmacy · 2020Article
- miR-552: an important post-transcriptional regulator that affects human cancer.Journal of Cancer · 2020Review
- EGFR, but not COX-2, protein in resected pancreatic ductal adenocarcinoma is associated with poor survival.Oncology letters · 2019Article
- MicroRNA-663b promotes cell proliferation and epithelial mesenchymal transition by directly targeting SMAD7 in nasopharyngeal carcinoma.Experimental and therapeutic medicine · 2018Article
- Indomethacin Disrupts Autophagic Flux by Inducing Lysosomal Dysfunction in Gastric Cancer Cells and Increases Their Sensitivity to Cytotoxic Drugs.Scientific reports · 2018Article
- Preoperative Neutrophil to Lymphocyte Ratio and Lymphocyte to Monocyte Ratio are Prognostic Factors in Gastric Cancers Undergoing Surgery.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2017Article
- DNA alterations in Cd133+ and Cd133- tumour cells enriched from intra-operative human colon tumour biopsies.BMC cancer · 2017Article
- Host knockout of E-prostanoid 2 receptors reduces tumor growth and causes major alterations of gene expression in prostaglandin EOncology letters · 2017Article
- MiR-17-5p promotes cancer cell proliferation and tumorigenesis in nasopharyngeal carcinoma by targeting p21.Cancer medicine · 2016Article
- Upregulation of nemo-like kinase is an independent prognostic factor in colorectal cancer.World journal of gastroenterology · 2015Article
- Hitting the Bull's-Eye in Metastatic Cancers-NSAIDs Elevate ROS in Mitochondria, Inducing Malignant Cell Death.Pharmaceuticals (Basel, Switzerland) · 2015Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Preclinical data, and an increasing list of clinical investigations, show anti-inflammatory agents to favourably influence the biology of colorectal tumor. We have earlier reported on re-expression of activated immune cells after three days preoperative treatment of patients with colorectal carcinoma, randomized to receive oral NSAID (indomethacin or celebrex). Antisecretory prophylaxis (esomeprasol) was provided to all patients and served as sham treatment. Concomittant to MHC locus activation, Prominin1/CD133, a marker associated with stemness and poor prognosis in several solid tumors, was downregulated. The aim of the present study was to evaluate expression of additional regulators belonging to the stem cell niche, OCT4, SOX2 and BMP7, as well as some microRNAs, reported to act as tumor suppressors or oncomiRs. Peroperative tumor biopsies were analyzed by microarrays, quantitative real-time PCR and immunohistochemistry (IHC). The stem cell master regulator SOX2 was increased by NSAIDs (p<0.01), as well as the tumor suppressor miR-630 (p<0.01), while BMP7, a marker for poor prognosis in CRC, was downregulated by NSAID (indomethacin, p<0.02). The upregulation of SOX2, but not of its heterodimer binding partner OCT4, could imply a negative feed-back loop, with a switch‑off for stemness preservation of tumor cells. This is supported by the overall evaluation of gene expression profiles with subsequent events, indicating less aggressive tumors following NSAID treatment.
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