The lipocalin saga: Insights into its role in cancer-associated cachexia

Abstract

Cancer-associated cachexia (CAC) is a debilitating condition, observed in patients with advanced stages of cancer. It is marked by ongoing weight loss, weakness, and nutritional impairment. Lower tolerance of chemotherapeutic agents and radiation therapy makes it difficult to treat CAC. Anorexia is a significant contributor to worsening CAC. Anorexia can be found in the early or advanced stages of cancer. Anorexia in cancer patients arises from a confluence of factors. Tumor-related inflammatory cytokines can directly impact the gastrointestinal tract, leading to dysphagia and compromised gut function. Additionally, increased serotonin and hormonal disruptions lead to early satiety, suppressing appetite. Due to the complexities in the pathogenesis of the disease, identifying druggable targets is a challenge. Research is ongoing to identify novel targets for the treatment of this condition. Recent research suggests a potential link between elevated levels of Lipocalin 2 (LCN2) and cachexia in cancer patients. LCN2, a glycoprotein primarily released by neutrophils, is implicated in numerous illnesses, including skin disorders, cancer, atherosclerosis, and type 2 diabetes. LCN2 suppresses hunger by binding to the melanocortin-4 receptors. Several in vitro, in vivo, and clinical studies indicate the association between LCN2 levels and appetite suppression. Further research should be explored emphasizing the significance of well-crafted clinical trials to confirm LCN2's usefulness as a therapeutic target and its ability to help cancer patients who are suffering from the fatal hallmark of cachexia. This review explores LCN2's function in the multifaceted dynamics of CAC and anorexia.