Abstract
Evodiamine is a natural alkaloid extracted from Fructus Evodia. This bioactive alkaloid has been reported to have a wide range of biological activities, including anti-injury, antiobesity, vasodilator, and anti-inflammatory effects. In recent years, it has been found that evodiamine has tumor-suppressive effects on a variety of tumors. There is growing evidence that evodiamine can inhibit the rapid proliferation of tumor cells, induce cell cycle arrest at a certain phase, increase the incidence of apoptosis, promote autophagy, inhibit microangiogenesis and migration, and regulate immunotherapy. Evodiamine can inhibit Wnt/β-catenin, mTOR, NF-κB, PI3K/AKT, JAK-STAT, and other signaling pathways in various cancer cells, and it can significantly downregulate the expression of many tumor markers, such as VEGF and COX-2. These facts partially explain the antitumor mechanism of evodiamine. In this article, the antitumor mechanism of evodiamine was reviewed to provide the basis for its clinical application and therapeutic development in the future.
Highlights
Introduction e traditional Chinese medicine FructusEvodia is the dry fruit of the plant Evodia rutaecarpa, and it was first mentioned in “Shennong Materia Medica Classic.” It has been found that E. rutaecarpa has analgesic, antidiarrheal, antiemetic, and antiinflammatory effects in clinical practice [1,2,3,4,5]. e dried, powdered fruit (2.5 kg) of E. rutaecarpa was defatted with n-hexane (2 × 5 L) and extracted with acetone (3 × 5 L) at room temperature to yield an extract (137 g). e crude acetone extract was eluted with n-hexane: acetone (9 : 1–19 :1) on a silica gel column to produce evodiamine (6.17 g) [6]
Evodiamine has been found to have antitumor activity against a variety of tumor cells, involving various mechanisms that cause cancer cell death, such as induction of cell cycle arrest, promotion of cell apoptosis, promotion of autophagy, and inhibition of tumor invasion and metastasis [23,24,25,26,27,28,29,30] (Figure 1). e signaling pathways involved in the antitumor effect of evodiamine include the classical apoptosis pathway, endoplasmic reticulum stress, MAPK, PI3K-Akt, and JAK-Signal transduction and activator of transcription (STAT) [31,32,33,34]
Liu et al further found that evodiamine could induce autophagy mediated by calcium/Junn terminal kinase (JNK) signals in glioma cells, while treatment with Ca2+ scavenger BAPTA-AM significantly inhibited the activation of the intracellular JNK pathway and decreased autophagy, while apoptosis was increased [62]. ese results confirm that evodiamine can promote Ca2+-mediated autophagy in the JNK pathway and that the inhibition of autophagy induced by this pathway can reduce the activity of tumor cells and promote apoptosis
Summary
Luning Li ,1 Cunxin Zhang ,2 Chen Huang ,1 Xinchen Tian ,3 Wenxue Sun ,1,4 and Shulong Jiang 1. Evodiamine has been found to have antitumor activity against a variety of tumor cells, involving various mechanisms that cause cancer cell death, such as induction of cell cycle arrest, promotion of cell apoptosis, promotion of autophagy, and inhibition of tumor invasion and metastasis [23,24,25,26,27,28,29,30] (Figure 1). E signaling pathways involved in the antitumor effect of evodiamine include the classical apoptosis pathway, endoplasmic reticulum stress, MAPK, PI3K-Akt, and JAK-STAT [31,32,33,34].
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
