TABLE 1.

Tabular representation of the reported functions.

Mechanism	Phenotype of anticancer effects
Caspase effect mechanism (cleaved-PARP↑, caspase-3↓, cleaved-caspase-3↑, Bax↑, Bcl-xL↓, Bcl-2↓, caspase-9↓, cleaved-caspase-9↑, cle-caspase-8↑, and cyt-c↑)	Cancer cell viability↓, cancer cell death, or apoptosis↑
MMP-2↓, MMP-9↓, and p-FAK↓	Cell migration and invasion↓
p53↑, c-Myc↓, and PI3k/AKT (Akt↓, p-Akt↓, and p-PI3Ks↓)	As a cancer suppressor gene, the p53 protein regulates the mechanism of apoptosis inhibition. As an oncogene, the activation of c-Myc causes excessive proliferation of cells. The PI3k/AKT signaling pathway plays an important role in apoptosis.
MAPK (p-MKK4↑,p-MKK3↑, p-JNKs↑, p-MEK↑, p-p38↑, and p-ERK1/2↑)	The ERK pathway is the most prominent and clinically utilized target, while the JNK pathway and p38 pathway play critical modulatory roles in cancer cells.
Autophagy (LC3-I↓, LC3-II↑, ROS↑, and mTOR↓)	Autophagy is a form of programmed cell death, and inducing autophagy may be an essential strategy against cancer.
PKC (PKC-α↓ and PKC-ϵ↓)	PKC can affect division and proliferation by catalyzing some small-molecule peptides and enzymes that bind to DNA in tumor cells.
ROS-mediated apoptosis (ER stress↑, ROS↑, p-STAT3↓, ATF4↑, and H2O2↑)	High levels of ROS can activate a variety of proapoptotic signaling pathways.
G-quadruplex	G-quadruplex has become one of the critical targets for developing antitumor drugs, and CHE has good selectivity for G-quadruplex while interacting with DNA
p21↑ and p27↑	Cell cycle arrest.
Mitochondria (mitochondrial membrane potential↓ and cyt-c↑, ROS↑)	The mitochondrial membrane potential is decreased, the permeability of the mitochondrial membrane is increased, and the proapoptotic factors are released into the cytoplasm.