AI Article Synopsis

  • Reactive oxygen species are by-products of normal cell metabolism essential for cell signaling and homeostasis, but imbalances can lead to oxidative stress and increase cancer risk.
  • The study focused on genes related to oxidative stress in endometrial cancer patients and explored their connections to miRNAs, using various molecular techniques for analysis.
  • Results indicated that while certain genes were overexpressed, their regulation by specific miRNAs was complex and varied, suggesting that targeting miRNAs could be a potential therapeutic strategy in managing oxidative stress in endometrial cancer.

Article Abstract

Reactive oxygen species are formed as by-products of normal cell metabolism. They are needed to maintain cell homeostasis and signaling, which is possible due to defense systems. Disruption of this balance leads to oxidative stress that can induce cancer. Redox regulation by miRNAs may be a potential therapeutic target. The aim of the study was to assess the activity of genes associated with oxidative stress in endometrial cancer and to determine their relationship with miRNAs. The study included 45 patients with endometrioid endometrial cancer and 45 without neoplastic changes. The expression profile of genes associated with oxidative stress was determined with mRNA microarrays, RT-qPCR and ELISA. The miRNA prediction was performed based on the miRNA microarray experiment and the mirDB tool. PRDX2 and AQP1 showed overexpression that was probably not related to miRNA activity. A high level of PKD2 may be the result of a decrease in the activity of miR-195-3p, miR-20a, miR-134. A SOD3 level reduction can be caused by miR-328, miR-363. In addition, miR-363 can also regulate KLF2 expression. In the course of endometrial cancer, the phenomenon of oxidative stress is observed, the regulation of which may be influenced by miRNAs.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9779631PMC
http://dx.doi.org/10.3390/ijms232415817DOI Listing

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