## 3 Pharmacological Properties of GP
### Anti-Cancer Effect
\begin{table}
\begin{tabular}{c c c c} \hline \hline
**Active Ingredient** & **Model** & **Mechanism** & **Ref.** \\ \hline GPS & Human tongue cancer SCC-4 cells & Induced ER stress and the production of reactive oxygen species and Ca2+, changed the ratio of Bcl-2 and Bax, followed by the dysfunction of mitochondria, caused cytochrome c release, activation of caspase-3; decreased the levels of cyclin D2 and cyclin E, increased the levels of Chk2, p53, p16, and p21, which led to G0/G1 arrest. \\ \hline GPS & Human lung carcinoma A549 cells & Induced an arrest at both S phase and G2/M phase, increased the expression of cyclin E and PCNA, decreased the expression of cyclin A and B; induced apoptosis, decreased the expression of Bcl-2 and increased the expression of Bax, activated caspase-3 and the downstream substrates, DFF45 and PARP-1. \\ \hline GPS & Human oral squamous carcinoma SAS cells & Inhibited the metastatic and invasive capacity of oral cancer cells, decreased the abundance of several proteins, including NF-kB, COX-2, ERK1/2, MMP-9, MMP-2, SOS, Ras, uPA, FAK, and Akt, decreased mRNA levels of MMP-2, MMP-7, and MMP-9. \\ \hline GPS & Human oral cancer SAS cells & Reduced the levels of CDC25A, cyclin E, cyclin A, and CDK2, increased the levels of p53 and p21, caused G0/G1 phase arrest; triggered apoptotic cell death, increased levels of Bax but inhibited the levels of Bcl-2 and Bcl-xl, stimulated the release of cytochrome c, AIF, and Endo G, increased the translocation of AIF, Endo G, and GADD153, increased protein levels of puma, CAD, caspase-9, and caspase-3, TRAIL, Fas, FasL, ATF-4, and GRP78 but reduced levels of XIAP. \\ \hline GPS & Human oral cancer HSC-3 cells & Decreased the depolarization of mitochondrial membrane potential, induced cell death, G2/M phase arrest, and apoptosis, altered gene expression such as the expression of GTP binding protein. \\ \hline GPS & Human hepatocellular carcinoma HepG2 cells & Inhibited HIF-1\(\alpha\) mRNA expression, as well as disturbing HepG2 migration and invasion. \\ \hline GPS & Human hepatocellular carcinoma & Up-regulated IP3R and SOC proteins (STIM1 and Orai1) and down-regulated SERCA protein, which led to increased extracellular Ca2+ influx and ER Ca2+ release and decreased ER Ca2+ uptake. This process perturbed intracellular calcium homeostasis and finally triggered Ca2+-dependent apoptosis. \\ \hline GPS & Human colon cancer SW620 cells & Caused cell membrane integrity damage, promoted ROS production, decreased \(\Delta\varphi_{\text{m}}\) level, induced apoptotic morphology such as cell shrinkage and chromatin condensation, initiated apoptotic response, inhibited cell migration. \\ \hline GPS & Human colon cancer SW620 cells & Caused cell membrane integrity damage, promoted ROS production, decreased \(\Delta\varphi_{\text{m}}\) level, induced apoptotic morphology such as cell shrinkage and chromatin condensation, initiated apoptotic response, inhibited cell migration. \\ \hline GPS & Human colon cancer SW480 cells & Increased the plasma membrane permeability of SW-480 cells, decreased the \(\Delta\varphi_{\text{m}}\) level significantly, increased the level of intracellular ROS level, produced DNA fragmentation and induced apoptosis, caused serious microfilament network collapse as well as the significant decrease in the number of microvilli. \\ \hline GPS and flavonoids & Prostate cancer PC-3 cells & Induced both S and G2/M phases arrest and cell apoptosis, increased the expression of Bad, Bax, and caspase 3, decreased the level of Bcl-2 and Bcl-xl, modulated the expression of G2 and M checkpoint regulators, cyclin A and B. \\ \hline \hline \end{tabular}
\end{table} 
Table 1: _Cont._
\begin{table}
\begin{tabular}{c c c c} \hline \hline  
Figure 4: The anti-cancer mechanisms of GP \(\uparrow\) meant up-regulation, \(\downarrow\) meant down-regulation.