The Role of the JNK Gene in Ovarian Cancer Inflammatory Pathways

Ovarian cancer, one of the leading causes of cancer-related deaths in women globally, presents a significant challenge due to its common late-stage diagnosis and chemoresistance (inability of the tumor to respond to drugs). The c-Jun N-terminal kinase (JNK) signaling pathway plays a crucial role in ovarian cancer progression, contributing to inflammation, tumor survival, metastasis, and chemotherapy resistance. This literature review examines the role of the JNK signaling pathway in ovarian cancer, with a focus on its role in inflammation, metastasis, and chemoresistance. JNK regulates key inflammatory cytokines, such as TNF-α and IL-6, which promote tumor growth and immune evasion. Moreover, it influences cellular processes including migration, invasion, and epithelial-to-mesenchymal transition (EMT), which are crucial for metastasis. JNK promotes chemoresistance by activating survival pathways that allow tumor cells to withstand chemotherapy-induced apoptosis. While JNK inhibitors show promise as a therapeutic strategy, several challenges remain, including selectivity, toxicity, and the development of resistance mechanisms. In vivo studies using patient-derived models are necessary to better understand JNK’s role in ovarian cancer and to refine therapeutic approaches. Additionally, personalized medicine strategies that identify specific molecular markers predicting response to JNK inhibition are crucial for optimizing treatment. Combining JNK inhibitors with chemotherapy or immune checkpoint blockage may be synergistic. Such combinations could improve outcomes and help overcome current therapeutic barriers.