Involvement of heat shock proteins and parkin/α-synuclein axis in Parkinson's disease.

Parkinson's disease (PD) is one of the most common neurological diseases, next only to Alzheimer's disease (AD) in terms of prevalence. It afflicts about 2-3% of individuals over 65 years old. The etiology of PD is unknown and several environmental and genetic factors are involved. From a pathological point of view, PD is characterized by the loss of dopaminergic neurons in the substantia nigra, which causes the abnormal accumulation of α-synuclein (α-syn) (a component of Lewy bodies), which subsequently interact with heat shock proteins (HSPs), leading to apoptosis. Apoptosis is a vital pathway for establishing homeostasis in body tissues, which is regulated by pro-apoptotic and anti-apoptotic factors. Recent findings have shown that HSPs, especially HSP27 and HSP70, play a pivotal role in regulating apoptosis by influencing the factors involved in the apoptosis pathway. Moreover, it has been reported that the expression of these HSPs in the nervous system is high. Apart from this finding, investigations have suggested that HSP27 and HSP70 (related to parkin) show a potent protective and anti-apoptotic impact against the damaging outcomes of mutant α-syn toxicity to nerve cells. Therefore, in this study, we aimed to investigate the relationship between these HSPs and apoptosis in patients with PD.

The potential role of nicotine in breast cancer initiation, development, angiogenesis, invasion, metastasis, and resistance to therapy.

A large body of research studying the relationship between tobacco and cancer has led to the knowledge that smoking cigarettes adversely affects cancer treatment while contributing to the development of various tobacco-related cancers. Nicotine is the main addictive component of tobacco smoke and promotes angiogenesis, proliferation, and epithelial-mesenchymal transition (EMT) while promoting growth and metastasis of tumors. Nicotine generally acts through the induction of the nicotinic acetylcholine receptors (nAChRs), although the contribution of other receptor subunits has also been reported. Nicotine contributes to the pathogenesis of a wide range of cancers including breast cancer through its carcinogens such as (4-methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and N-nitrosonornicotine (NNN). Current study aims to review the mechanistic function of nicotine in the initiation, development, angiogenesis, invasion, metastasis, and apoptosis of breast cancer with the main focus on nicotine acetylcholine receptors (nAChRs) and nAChR-mediated signaling pathways as well as on its potential for the development of an effective treatment against breast cancer. Moreover, we will try to demonstrate how nicotine leads to poor treatment response in breast cancer by enhancing the population, proliferation, and self-renewal of cancer stem cells (CSCs) through the activation of α7-nAChR receptors.