Guest Editors
Rick Francis Thorne, The University of Newcastle, Australia. E-mail: rick.thorne@newcastle.edu.au; rickfthorne@gmail.com
Ihtisham Bukhari, Fifth Affiliated Hospital of Zhengzhou University, China. E-mail: bukhari@zzu.edu.cn; bukhari5408@gmail.com
Muhammad Riaz Khan, Centre Hospitalier Universitaire de Sherbrooke, Canada. E-mail: Muhammad.Riaz.Khan@usherbrooke.ca
Summary
Metastasis is a complex multi-step process involving the sequential invasion of cancer cells into the circulation or lymphatics to later arrest and establish secondary lesions at distal sites. Notably, cancer cells transiting to secondary sites may not proliferate immediately, often remaining dormant until conditions are congenial to resume proliferation. The mechanisms underlying metastatic spread, including the orchestrated programs coordinating cell migration and dissemination throughout disease progression, remain unclear. Nevertheless, it is generally acknowledged that tumor tissues possess unique characteristics that help promote cancer progression, including low oxygen tension or hypoxia. Tumor hypoxia results from oxygen deprivation to the tissue as rapid tumor growth outstrips oxygen supplies limiting circulation. It represents a common feature of most solid cancers, broadly shaping the tumor microenvironment and eliciting a spectrum of actions on cancer and non-cancer cells alike to enable cancer progression. For example, effects range from promoting angiogenesis in endothelial cells to metastasis of cancer cells through facilitating the EMT process. Moreover, the case can be made that the hypoxic environment within tumors also negatively influences most cancer therapies, including radiotherapy, chemotherapy, and immunotherapy. It is observed that drug-resistant cancer cells possess more mitochondria, consume more oxygen than non-resistant cells, and produce significantly higher levels of ROS. Consequently, targeting tumor hypoxia has arisen as a promising therapeutic strategy but despite its overall prominence in cancer biology, no standard of care has yet been effectively established to reduce the impact of hypoxia. Areas of hypoxia occur heterogeneously throughout tumors although, broadly speaking, hypoxia increases the levels of reactive oxygen species (ROS), disrupting cellular homeostasis through oxidative stress and mitochondrial dysfunction. In both transformed and non-transformed cells alike, these insults can initiate cell death pathways, including apoptosis, autophagy, necroptosis, pyroptosis, ferroptosis, and oxytosis. ROS accumulation also triggers many important cellular stress responses, including DNA damage responses and other signal transduction-related responses. Nevertheless, cancer cells co-exist and appear to benefit from heightened ROS levels. In this condition, tumors no longer depend on glucose metabolism for energy and utilize classic aerobic glycolysis (Warburg effect); thus, switching to oxidative metabolism (OXMET), tumor cells increase cellular energy or metabolic demand outstrip the glutamine or other amino acids supply for survival. As said, targeting hypoxia can improve the therapeutic response in cancer but much more need to be done. Not many studies have shown the relationship between hypoxia and cancer metastasis, the anti-hypoxic effects of anticancer drugs/therapies, and the underlying mechanism of cancer inhibition. This Special Issue aims to provide a broad and updated overview of the relationship between various types of cell death and oxidative stress and cancer metastasis. We especially welcome original research papers (in vitro, in vivo, or phase II trials) or systematic or meta-analytic reviews addressing unique technological advances to treat cancer metastasis by using targeted therapy and the well-being of cancer patients after primary treatment in the below-mentioned areas.
Potential topics include but are not limited to the following:
· Hallmarks of cancer metastasis.
· Epithelial-mesenchymal transition in cancer metastasis: mechanism and its clinical importance.
· Cancer metastasis treatment using target therapy.
· Suppression of signal transduction to inhibit the growth of metastasis.
· Molecular mechanism of inflammasome activation and pyroptosis in cancer.
· Novel molecular mechanisms and crosstalk between cell death and oxidative stress.
· Crosstalk between endoplasmic reticulum (ER) stress, oxidative stress, and cancer.
Keywords
Hypoxia, Metastasis, Anticancer, Cancer management, Cancer Diagnosis, Cancer Biomarkers
Login
Register
Submit a Paper
Propose a Special lssue