The Role of PTEN Tumor Suppressor Genes in Endometrial Cancer

Introduction: The PTEN gene is one of the main tumour suppressors, which is essential in regulating cell growth and preventing carcinogenesis. In endometrial cancer, mutations or loss of function of PTEN are frequently associated with disease progression, making this gene a relevant target for studies on molecular mechanisms and potential therapeutic approaches. Uncontrolled activation of the PI3K/AKT pathway, resulting from PTEN inactivation, favours cell proliferation and resistance to apoptosis, contributing to tumour aggressiveness. Methology: This study is based on a systematic review of the scientific literature, analysing articles published between 2010 and 2025 in databases such as PubMed, Scopus and Web of Science. Studies that investigate the relationship between PTEN mutations and the development of endometrial cancer, considering molecular, clinical and therapeutic aspects, were included. The selection of articles followed strict inclusion and exclusion criteria, prioritising research with significant samples and well-established methodologies. Results: The data analysed indicate that PTEN mutations are present in approximately 50% of endometrial cancer cases, being more frequent in high-grade tumours. These mutations compromise the function of the PTEN protein, allowing cells with DNA damage to avoid apoptosis and continue to proliferate. In addition, tumours with PTEN mutations are more resistant to conventional treatments, such as chemotherapy and radiotherapy. Recent studies suggest that inhibition of the PI3K/AKT pathway may be a promising strategy to contain tumour progression in patients with PTEN mutations. Discussion: The presence of PTEN mutations in endometrial cancer reinforces its importance as a prognostic and therapeutic biomarker. Uncontrolled activation of the PI3K/AKT pathway contributes to exacerbated cell proliferation, resistance to apoptosis, and tumour angiogenesis, favouring cancer dissemination. Therapeutic strategies aimed at modulating this pathway are being investigated, including specific PI3K inhibitors and targeted therapies. However, challenges such as heterogeneity of mutations and the interaction of PTEN with other molecular pathways require more personalised approaches for the treatment of the disease. Conclusion: The PTEN gene plays an essential role in regulating cell growth and preventing endometrial cancer. Its mutation or loss of function is directly related to tumour progression, therapeutic resistance, and poor prognosis of the disease. Understanding these mechanisms paves the way for the development of new therapeutic strategies, including targeted therapies and PI3K/AKT pathway inhibitors, which may improve clinical outcomes for patients. Future studies should focus on identifying biomarkers associated with PTEN and improving targeted therapies to optimise the management of endometrial cancer