Abstract
The development of cancer is a problem that has accompanied mankind for years. The growing number of cases, emerging drug resistance, and the need to reduce the serious side effects of pharmacotherapy are forcing scientists to better understand the complex mechanisms responsible for the initiation, promotion, and progression of the disease. This paper discusses the modulation of the particular stages of carcinogenesis by selected physiological factors, including: acetylcholine (ACh), peroxisome proliferator-activated receptors (PPAR), fatty acid-binding proteins (FABPs), Bruton’s tyrosine kinase (Btk), aquaporins (AQPs), insulin-like growth factor-2 (IGF-2), and exosomes. Understanding their role may contribute to the development of more effective and safer therapies based on new binding sites.
Highlights
The increasing prevalence of various types of cancers is a global phenomenon that has been occurring widely and affecting increasing numbers of people
The high activity of cyclooxygenase affects the inactivation of the PTEN protein [34, 35], whose biological role is silencing PI3K/Akt pathway signaling. This leads to cellular signal transition and induces effects that contribute to the enhanced growth and proliferation of cancer cells as well as inhibits the process of their death
By supplying long chain fatty acids, FABP5 leads to PPARγ activation [75,76,77,78]
Summary
The increasing prevalence of various types of cancers is a global phenomenon that has been occurring widely and affecting increasing numbers of people. The high activity of cyclooxygenase affects the inactivation of the PTEN protein [34, 35], whose biological role is silencing PI3K/Akt pathway signaling This leads to cellular signal transition and induces effects that contribute to the enhanced growth and proliferation of cancer cells as well as inhibits the process of their death. By supplying long chain fatty acids, FABP5 leads to PPARγ activation [75,76,77,78] Stimulation of these receptors results in increased expression of vascular endothelial growth factor (VEGF), thereby accelerating the angiogenesis process. This mechanism plays a key role in the development of castration-resistant prostate cancer [79,80,81]. Tipifarnib as a monotherapy of metastatic head and neck squamous cell carcinoma (HNSCC) bearing HRAS mutation in the II phase of clinical trial showed durable response and lack of progression in most of the patients [204]
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