Abstract
Background. Type 2 diabetes mellitus, obstructive sleep apnea, osteoarthritis and certain types of cancer are known to correlate with obesity. The mechanisms underlying the link between metabolic disorders and cancer remain obscure, yet assuming a potentially important role of reduced insulin sensitivity, altered glucose metabolism in tumor cells (the so-called Warburg effect), changes in the spectrum of secreted adipokines or interaction with their cognitive receptors as well as changes in steroid sex hormone production.Material and methods. A search for articles published in peer-reviewed journals indexed in pubmed, Wos, scopus and Rsci was carried out. More than 150 articles devoted to the study of the relationship between metabolic disorders and tumor progression were analyzed, of which 69 were included in this review.Results. The main strategy of anticancer therapy is to suppress the proliferation of tumor cells and metastasis. However, one should take into consideration a significant role of additional factors that can enhance side effects of anticancer therapy, ensure the resistance of tumor cells to chemotherapy or change cancer cell metabolic profile. New data recently emerging in the literature indicate an important function of proteins such as t-cadherin and urokinase receptor (upar) and their possible involvement in the regulation of tumor cell metabolism, in particular, sensitivity to insulin and adipose tissue hormones. The review encompasses recent data on the involvement of t-cadherin and upar in the regulation of metabolism and proposes a model explaining the relationship between these proteins and metabolic disorders associated with the processes of carcinogenesis and chemoresistance of cancer cells.Conclusion. Understanding of the factors and mechanisms that support obesity and metabolic disorders is relevant both for the development of cancer preventive measures and optimization of therapeutic strategies for combating cancer.
Highlights
Type 2 diabetes mellitus, obstructive sleep apnea, osteoarthritis and certain types of cancer are known to correlate with obesity
The mechanisms underlying the link between metabolic disorders and cancer remain obscure, yet assuming a potentially important role of reduced insulin sensitivity, altered glucose metabolism in tumor cells, changes in the spectrum of secreted adipokines or interaction with their cognitive receptors as well as changes in steroid sex hormone production
One should take into consideration a significant role of additional factors that can enhance side effects of anticancer therapy, ensure the resistance of tumor cells to chemotherapy or change cancer cell metabolic profile
Summary
Обусловливающие взаимосвязь метаболических нарушений с возникновением злокачественных опухолей, пока неизвестны; значительную роль может играть изменение чувствительности к инсулину и факторам роста, изменение спектра секретируемых адипокинов или особенности их взаимодействия с рецепторами, изменение содержания стероидных половых гормонов в организме, а также особенности метаболизма глюкозы в опухолевых клетках (так называемый эффект Варбурга). Что значительную роль в этих процессах играет ряд факторов, способных усиливать побочные эффекты противоопухолевой терапии, поддерживать резистентность опухолевых клеток или изменять их метаболический профиль. Имеются новые данные о функции таких белков, как Т-кадгерин и рецептор урокиназы (uPAR), и их возможном участии в регуляции метаболизма опухолевых клеток, в частности чувствительности к инсулину и гормонам жировой ткани. Предложена модель, объясняющая взаимосвязь этих белков и метаболических нарушений, ассоциированных с процессами канцерогенеза и химиорезистентности опухолевых клеток. THE RELATIONSHIP BETWEEN METABOLIC DISORDERS AND TUMOR PROGRESSION: REVIEW OF PRESENT DATA
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