Role of HSP60/HSP10 in Lung Cancer: Simple Biomarkers or Leading Actors?

Abstract

Cancers are one of the major challenges faced by modern medicine both because of their impact in terms of the amount of cases and of the ineffectiveness of therapies used today. A concrete support to the fight against them can be found in the analysis and understanding of the molecular mechanisms involving molecular chaperones. In particular, HSP60 and HSP10 seem to play an important role in carcinogenesis, supporting tumours in their proliferation, survival, and metastasis. Efforts must be directed toward finding ways to eliminate or block this “mistaken” chaperone. Therefore, the scientific community must develop therapeutic strategies that consider HSP60 and HSP10 as the possible target of an anti-tumoural treatment and not only as diagnostic biomarkers, since they contribute to the evolution of pre-cancerous respiratory pathologies in lung tumours. HSP60 acts at the mitochondrial, cytoplasmic, and extracellular levels in the development of cancer pathologies. The molecular mechanisms in which these chaperones are involved concern cell survival, the restoration of a condition of absence of replicative senescence, the promotion of pro-inflammatory environments, and an increase in the ability to form metastases. In this review, we will also present examples of interactions between HSP60 and HSP10 and different molecules and ways to exploit this knowledge in anticancer therapies for lung tumours. In order to improve not only chances for an earlier diagnosis but also treatments for patients suffering from this type of disease, chaperones must be considered as key agents in carcinogenesis and primary targets in therapeutics.