Table 1.

Summary of the in vitro chemopreventive, anticancer, and antimetastatic effects of RSV and PD against OSCC-related cancer cell lines: tested concentrations, times, employed cells, markers, and general results.

In Vitro Concentrationsand Times	Cell Lines	Markers	Results	Reference
5, 10, 25, 50, and 100 µM, for 24, 48, and 72 h	PE/CA-PJ15		Dose-dependent cytotoxicity. Prolongation of the S phase of the cell cycle (50–100 µM). Reduction in cell migration ability (25–100 µM).	Atienzar et al. [34]
From 0.1 to 1.5 μg/mL, for 48 h	SCC-VII SCC-25 YD-38	Myt1,cdc2 proteins	Dose-dependent cytotoxicity. IC50 values: 0.5–1 μg/mL. Cell cycle interruption (48 h treatment) by the upregulation of Myt1 and the phosphorylation of cdc2. Promotion of cell apoptosis.	Yu et al. [35]
25, 50, and 100 μM, for 5 h	KB		An RSV concentration of 100 μM significantly reduced cell adhesion and migration.	Shan et al. [36]
30–300 µM, for a maximum of 72 h	KB	Procaspase-3, -7, and -9, caspase-3	IC50 values: 197.4 and 63.3 µM after 12 and 72 h treatments, respectively. Pro-apoptotic activity by internucleosomal DNA fragmentation as well as the cleavage of procaspase-3, -7, and -9, and caspase-3.	Kim et al. [37]
10–500 µM, for 24, 48, and 72 h	Cal27 SCC25 SCC15	MPP, Bax, Bak, bcl-2, bcl-XL, cytochrome c, caspase-3, caspase-9, and EMT transcription factor	IC50 values: 100 µM against Cal27 (24 h treatment), 200 µM against SCC15 (72 h treatment), and 300 µM against SCC25 (72 h treatment). Proapoptotic effect by the modulation of several factors: MMP, Bax, Bak, bcl-2 and bcl-XL, cytochrome c, and caspases. Reduction in cell migration by the inhibition of the EMT transcription factor.	Kim et al. [38]
25 µM, for 1 h	YD-10B	TWIST, SLUG	Downregulation of EMT transcription factors, resulting in the reduction in the number of invading cells when compared with the positive control (LPA).	Kim et al. [39]
Up to 25 µM	YD-9YD-10B YD-38	MT1-MMP, Zeb1	Dose-dependent reduction in cell invasion. Suppression of MT1-MMP and Zeb1 expression.	Kim et al. [40]
10, 20, 50, and 100 µM, for 48 h	Cal-27	MAGEA12/Akt pathway	Dose-dependent reduction in cell viability and the MAGEA12/Akt cascade. IC50 value: 50 µM. Slightly decreased effect against cells overexpressing MAGEA12.	Shang et al. [41]
Coadministration with CUR at 6.2, 12.5, 25, and 50 μM, for 48 h	Cal-27 SCC-15 FaDU		Dose-dependent cytotoxicity, which was enhanced with the coadministration of the two polyphenols.	Masuelli et al. [42]
10, 20, 50, and 75 µM, for 24 h	Cisplatin-resistant Cal-27	ERK, p-38, MMP-2, and MMP-9	Reduced cytotoxicity in cisplatin-resistant cells. Dose-dependent antimetastatic effects. Inhibition of ERK and p-38 phosphorylation, as well as the downregulation of MMP-2 and -9 expression.	Chang et al. [43]
20 μM, or 24 h	SAS Sa3 HSC-3	EGFR ERK1/2 uPAR	Increased level of phosphorylated ERK1/2. Downregulation of integrin β1 and uPAR expression.	Uzawa et al. [44]
PD up to 2 mM, for 24 and 72 h	Ca9-22 Cal-27 Keratinocites	Cytochrome c, bcl-2, bax, ATG5, LC3, E-cadherin, N-cadherin, SLUG, and Snail	Dose-dependent cytotoxicity against cancer cells. Cytocompatibility against healthy cells (keratinocites) at the tested concentrations.IC50 values: 1.15 and 0.95 mM for Cal-27 and Ca9-22 cells, respectively. Proapoptotic effect via the release of cytochrome c, decrease in bcl-2 synthesis, and increase in bax expression. Autophagy induction by the stimulation of ATG5 and LC3 expression. Antimetastatic effect by increasing E-cadherin expression and the suppression of Snail and Slug proteins.	Bang et al. [45]