An Overview of the Potential Antineoplastic Effects of Casticin

Molecules. 2020 Mar 12;25(6):1287. doi: 10.3390/molecules25061287.

Abstract

Cancer persists as one of the leading causes of deaths worldwide, contributing to approximately 9.6 million deaths per annum in recent years. Despite the numerous advancements in cancer treatment, there is still abundant scope to mitigate recurrence, adverse side effects and toxicities caused by existing pharmaceutical drugs. To achieve this, many phytochemicals from plants and natural products have been tested against cancer cell lines in vivo and in vitro. Likewise, casticin, a flavonoid extracted from the Vitex species, has been isolated from the leaves and seeds of V. trifolia and V. agnus-castus. Casticin possesses a wide range of therapeutic properties, including analgesic, anti-inflammatory, antiangiogenic, antiasthmatic and antineoplastic activities. Several studies have been conducted on the anticancer effects of casticin against cancers, including breast, bladder, oral, lung, leukemia and hepatocellular carcinomas. The compound inhibits invasion, migration and proliferation and induces apoptosis (casticin-induced, ROS-mediated and mitochondrial-dependent) and cell cycle arrest (G0/G1, G2/M, etc.) through different signaling pathways, namely the PI3K/Akt, NF-κB, STAT3 and FOXO3a/FoxM1 pathways. This review summarizes the chemo-preventive ability of casticin as an antineoplastic agent against several malignancies.

Keywords: FOXO3a/FoxM1; NF-κB; PI3K/Akt; STAT3; apoptosis; cancer; casticin; flavonoid.

Publication types

  • Review

MeSH terms

  • Apoptosis / drug effects
  • Caenorhabditis elegans Proteins / genetics
  • Cell Cycle Checkpoints / drug effects
  • Cell Proliferation / drug effects*
  • Flavonoids / therapeutic use*
  • Forkhead Transcription Factors / genetics
  • Humans
  • Mitochondria / drug effects
  • Neoplasms / classification
  • Neoplasms / drug therapy*
  • Neoplasms / pathology
  • STAT3 Transcription Factor / genetics
  • Signal Transduction / drug effects

Substances

  • Caenorhabditis elegans Proteins
  • FOXO3a protein, C elegans
  • Flavonoids
  • Forkhead Transcription Factors
  • STAT3 Transcription Factor
  • STAT3 protein, human
  • casticin