European journal of dentistry · 2026
Ethanol Extract of Catharanthus roseus Leaves Exhibits Anticancer Effects on HSC-3 Tongue Cancer Cells Associated with PI3K Suppression and PARP Cleavage.
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Sandra Ferry, Djamil Melanie Sadono, Rizal Muhammad Ihsan, Hayuningtyas Ria Aryani, Dipankara Jackson, Isnaeni Nur'amalia, Krisdianto Samuel Ryan, Mochtar Kerinillia, Lee Kyung Hoon
Аннотация
OBJECTIVE: Tongue cancer represents nearly half of all oral cancer cases globally, necessitating the exploration of novel therapeutic agents. Catharanthus roseus, known for its well-established anticancer properties, offers a promising alternative. Although C. roseus has been studied in several cancer models, its effects in tongue cancer cells, particularly in relation to phosphatidylinositol-3-kinase (PI3K) and poly(adenosine diphosphate-ribose) polymerase (PARP) pathways, have not been evaluated. This study examined the effect of the ethanol extract of C. roseus leaf (EECRL) on HSC-3 cells.
MATERIALS AND METHODS: Cells were treated with various concentrations of EECRL. Cell viability was assessed using the MTT assay, apoptosis was evaluated by sub-G1 analysis, and levels of cleaved-PARP and phosphorylated PI3K were measured using enzyme-linked immunosorbent assay.
STATISTICAL ANALYSIS: Data normality was assessed using the Shapiro-Wilk test. Depending on data distribution, comparisons were performed using one-way analysis of variance followed by Tukey's post hoc test or the Kruskal-Wallis test followed by Dunn's post hoc test. Correction for multiple comparisons was applied using the Holm-Bonferroni method, and adjusted p-values were used to determine statistical significance.
RESULTS: EECRL reduced number of viable cells and induced apoptosis in HSC-3 cells in a significant, concentration-dependent manner (adjusted p-value < 0.05). Additionally, EECRL significantly decreased the activity of PI3K in a concentration-dependent manner (adjusted p-value < 0.05) and significantly increased cleaved-PARP compared with the untreated group (adjusted p-value < 0.05).
CONCLUSION: EECRL reduced viable cell numbers and induced apoptotic features in HSC-3 tongue cancer cells, with effects associated with suppression of PI3K signaling and increased PARP cleavage. These findings suggest that EECRL may have potential as an alternative therapeutic candidate for tongue cancer. However, further mechanistic studies are required to confirm causal pathway involvement.
MATERIALS AND METHODS: Cells were treated with various concentrations of EECRL. Cell viability was assessed using the MTT assay, apoptosis was evaluated by sub-G1 analysis, and levels of cleaved-PARP and phosphorylated PI3K were measured using enzyme-linked immunosorbent assay.
STATISTICAL ANALYSIS: Data normality was assessed using the Shapiro-Wilk test. Depending on data distribution, comparisons were performed using one-way analysis of variance followed by Tukey's post hoc test or the Kruskal-Wallis test followed by Dunn's post hoc test. Correction for multiple comparisons was applied using the Holm-Bonferroni method, and adjusted p-values were used to determine statistical significance.
RESULTS: EECRL reduced number of viable cells and induced apoptosis in HSC-3 cells in a significant, concentration-dependent manner (adjusted p-value < 0.05). Additionally, EECRL significantly decreased the activity of PI3K in a concentration-dependent manner (adjusted p-value < 0.05) and significantly increased cleaved-PARP compared with the untreated group (adjusted p-value < 0.05).
CONCLUSION: EECRL reduced viable cell numbers and induced apoptotic features in HSC-3 tongue cancer cells, with effects associated with suppression of PI3K signaling and increased PARP cleavage. These findings suggest that EECRL may have potential as an alternative therapeutic candidate for tongue cancer. However, further mechanistic studies are required to confirm causal pathway involvement.