PHARMACOLOGICAL EFFECTS OF ERIANIN AND ITS DERIVATIVES ON THE TUMOR MICROENVIRONMENT: CURRENT PERSPECTIVES

Cancer development is determined not only by genetic and epigenetic alterations in tumor cells but also by complex interactions with the tumor microenvironment (TME). The TME consists of cancer-associated fibroblasts (CAFs), tumor-associated macrophages (TAMs), endothelial cells, immune cells, extracellular matrix, and various signaling molecules. These components play important roles in tumor proliferation, angiogenesis, invasion, metastasis, immune evasion, and the development of drug resistance [2,3]. Erianin is a naturally occurring dibenzyl compound isolated from plants belonging to the genus Dendrobium and has attracted considerable scientific interest in recent years due to its broad pharmacological properties, particularly its antitumor, antiangiogenic, immunomodulatory, and anti-inflammatory activities [1,2]. Available evidence indicates that erianin may affect several signaling pathways, including ROS/JNK, PI3K/AKT, JAK/STAT3, HIF-1α/PD-L1, mTOR, and Wnt/β-catenin [1,2]. In addition, experimental studies have demonstrated that erianin can inhibit angiogenesis, enhance the ability of macrophages to phagocytose tumor cells, and modulate the immune microenvironment [4–7]. The poor water solubility and limited bioavailability of erianin represent major factors restricting its pharmaceutical development and necessitate the development of novel derivatives and drug delivery systems [1,2]. This review analyzes the effects of erianin and its derivatives on the tumor microenvironment, their major molecular mechanisms, potential mechanisms of interaction with CAFs and TAMs, and future pharmacological perspectives.