Stress Response Signaling in Tumor Development and its Implications for Cancer Treatment

Homeostasis is key to the health and survival of all organisms. Environmental stress is ubiquitous and unavoidable to all living beings. A wide variety of stressors, such as ionizing radiation, prooxidants, nutrition deprivation, iron deficiency, viral infection, lipid overload, mechanical stress, and proteotoxic aggregates threaten to disrupt cell functions. Organisms develop evolutionarily conserved homeostatic programs including unfolded protein response (UPR), oxidative stress response, and integrated stress response (ISR) to restore homeostasis or adapt to the stress. When the stress is severe, prolonged, or the stress response signaling is dysregulated, it leads to tissue injury, metabolic dysfunction, and inflammation that increase the risk for pathological disorders, particularly, cancer. Thus, dysregulated stress response signaling contributes to all cancer hallmarks.

Cancer is one of the major health challenges worldwide, and dysregulated stress response signaling is considered a cancer hallmark. The mechanisms of dysregulated stress pathways leading to carcinogenesis, tumor growth, and metastasis is are yet largely unknown, and uncovering the missing links would reveal new ways for cancer prevention and treatment. Cancer treatments, including chemotherapy, radiotherapy, immunotherapy, and targeted therapy, as well as their combinations often cause stress to cancer cells and normal tissues. In addition, stress signaling affects the effectiveness of cancer treatment. Understanding the details of the dysregulation of various stress-signaling pathways that lead to cancer and their involvement in cancer treatment will provide us with new insights into tumor development and cancer therapy. This topic aims to address all aspects of dysregulated stress response signaling regulating cancer development and progression, as well as their implications for cancer treatment.

This topic welcomes articles investigating stress response signaling in all aspects of cancers, including but not limited to cancer biochemistry, cell biology, immunology, pathology and cancer treatment. Original Research articles and Review articles, as well as meta-analyses with the support of experimental data are encouraged.

Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.