Ovarian carcinoma is the leading cause of gynecological cancer-related death, still with a dismal five-year prognosis, mainly due to late diagnosis and the emergence of resistance to cytotoxic and targeted agents. Bcl-2 family proteins have a key role in apoptosis and are associated with tumor development/progression and response to therapy in different cancer types, including ovarian carcinoma. In tumors, evasion of apoptosis is a possible mechanism of resistance to therapy. BH3 mimetics are small molecules that occupy the hydrophobic pocket on pro-survival proteins, allowing the induction of apoptosis, and are currently under study as single agents and/or in combination with cytotoxic and targeted agents in solid tumors. Here, we discuss recent advances in targeting anti-apoptotic proteins of the Bcl-2 family for the treatment of ovarian cancer, focusing on BH3 mimetics, and how these approaches could potentially offer an alternative/complementary way to treat patients and overcome or delay resistance to current treatments.
Keyphrases
- cell death
- cell cycle arrest
- endoplasmic reticulum stress
- oxidative stress
- cancer therapy
- end stage renal disease
- ejection fraction
- newly diagnosed
- chronic kidney disease
- peritoneal dialysis
- prognostic factors
- papillary thyroid
- anti inflammatory
- stem cells
- squamous cell carcinoma
- pi k akt
- drug delivery
- mesenchymal stem cells
- cell therapy
- squamous cell
- cell proliferation
- signaling pathway
- ionic liquid
- lymph node metastasis
- replacement therapy