Introduction:

Bisphenol A (BPA) is a chemical to which humans are extensively exposed orally, inhaled and transdermally.

Justification:

Given the importance of the oncological pathology that may be associated with exposure to this chemical, it is essential to better understand its possible mechanisms of action associated with carcinogenesis.

Objective:

To investigate the carcinogenic mechanism associated with BPA exposure.

Results:

Although the majority of investigations have been oriented towards the endocrine disrupting effect, with the limitation that in vivo studies are carried out in animals, recent studies have shown that they can be carcinogenic in human tissues. However, more research is required on the role of low-dose BPA (as occurs under normal environmental conditions) and its effect on the regulation of global changes in gene expression and epigenetic alterations in cells, which allow establishing links with carcinogenesis; this review shows that the studies carried out to date point to several factors that may be involved, such as mutagenic effects that include changes in gene transcription and enzymes that promote cell proliferation, limiting apoptosis and promoting angiogenesis and migration of tumor cells.

Conclusion:

Although it is currently recognized that the cancer cell acquires pathological characteristics that help it to survive in the organism, these characteristics are due to genetic and epigenetic molecular mechanisms, many of which have been described for the case of human exposure to BPA.

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