Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P42345 (mTOR)
 26,049 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chemoprevention is suitable for patients who are at high risk of development of numerous or invasive nonmelanoma skin cancers (NMSCs). Various substances have been studied as potential chemopreventive agents for NMSC. Oral retinoids have been proven to be effective in the suppression of new squamous cell carcinoma (SCC) development. Patients need to stay on oral retinoids as long as chemoprevention is needed with careful monitoring of the dose and side effects. Topical retinoids are not effective in prevention of NMSC. In organ transplant patients with aggressive or numerous skin cancers, decrease in the immunosuppression or switch to mammalian target of rapamycin inhibitors (sirolimus or everolimus) can be considered. Field therapy for areas of severe actinic damage with photodynamic therapy, imiquimod, 5-fluorouracil, ingenol mebutate, or diclofenac sodium may theoretically decrease the risk of SCC through treatment of precancerous changes. However, there is limited data regarding efficacy of these agents in chemoprevention of NMSC. Epidemiologic studies suggest a protective role for nonsteroidal anti-inflammatory agents in development of NMSC. Limited data support chemopreventive effect of difluoromethylornithine and T4 endonuclease V for actinic keratoses and basal cell carcinoma. Amongst dietary factors, low-fat diet, limonene from citrus fruit peel, and caffeine may protect against NMSC.
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PMID:Chemoprevention of nonmelanoma skin cancer. 2553 38

Non-small-cell lung cancer (NSCLC) is the most common cause of cancer-associated mortality worldwide. MicroRNAs (miRs) are a class of small non-coding RNAs that are commonly dysregulated in human cancer. The aim of the current study was to evaluate the effect of miR-296-3p on the cell migration and invasion of NSCLC. Pairs of tumor tissues and para-cancerous tissues (n=50) were collected from patients with NSCLC, and the expression of miR-296-3p was analyzed by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Additionally, tumor cell viability, migration and invasion were examined in vitro using Cell Counting Kit-8, wound healing and Matrigel assays, respectively. Furthermore, potential targets of miR-296-3p were screened for using TargetScan and validated using a dual-luciferase reporter assay. The expression levels of phosphoinositide-3-kinase (PI3K), AKT serine/threonine kinase (AKT), mammalian target of rapamycin (mTOR), matrix metallopeptidase 2 (MMP2) and SRY-box 4 (SOX4) were detected by RT-qPCR and western blot analysis. The data indicated that miR-296-3p was downregulated in tumor tissues compared with adjacent normal tissues. Overexpression of miR-296-3p inhibited NSCLC cell viability, migration and invasion in vitro. Furthermore, apurinic/apyrimidinic endodeoxyribonuclease 1 (APEX1) was identified as a direct target of miR-296-3p. APEX1 expression was upregulated in tumor tissues compared with para-cancerous tissues, and the mRNA and protein expression levels of APEX1 were decreased following transfection of NSCLC cells with miR-296-3p mimics compared with control cells. Additional investigations revealed that miR-296-3p was involved in regulating the PI3K/AKT/mTOR signaling pathway, and miR-296-3p mimics decreased the mRNA and protein expression levels of MMP2 and SOX4. In summary, the findings demonstrated that miR-296-3p may function as a tumor suppressor, and inhibits the migration and invasion of NSCLC cells by targeting APEX1. miR-296-3p is therefore a potential therapeutic molecular modulator of NSCLC.
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PMID:miR-296-3p targets APEX1 to suppress cell migration and invasion of non-small-cell lung cancer. 3140 54