Anticancer Activity and Apoptotic Induction of C. Fruticosa Leaf against HeLa cell Lines

Abstract

Cervical cancer remains one of the most prevalent cancers among women worldwide and continues to pose a major global health challenge. Despite advances in treatment, the limitations and adverse effects of conventional therapies emphasize the need for safer and more effective anticancer agents derived from natural sources. This study investigated the anticancer potential of Cordyline fruticosa leaf methanolic extract against cervical cancer (HeLa) cells by analyzing its phytochemical composition, cytotoxic activity, and ability to induce apoptosis. High-Performance Liquid Chromatography (HPLC) was used to identify the extract’s flavonoid content. Five major flavonoids were detected: Rutin (35.2%), Luteolin (20.1%), Kaempferol-3-O-glucoside (17.8%), Apigenin (14.6%), and a Myricetin derivative (8.3%). These compounds are known for their antioxidant and anticancer properties, suggesting that C. fruticosa is a promising source of bioactive phytochemicals. Cytotoxic activity was evaluated using the MTT assay. HeLa cells treated with extract concentrations ranging from 0–100 µg/mL for 48 hours exhibited a dose-dependent reduction in cell viability, with an IC₅₀ value of 21.58 µg/mL, indicating a high cytotoxicity. One-way ANOVA showed significant differences among treatment groups (p < 0.001), confirming the extract’s inhibitory effect on cancer cell proliferation. To determine the mechanism underlying this cytotoxic effect, apoptosis was assessed using TUNEL and Annexin V/PI staining. The TUNEL assay revealed increased DNA fragmentation at higher extract concentrations. Flow cytometry analysis further demonstrated concentration-dependent apoptosis, with apoptotic cell percentages of 24.3%, 46.7%, and 71.2% at 25 µg/mL, 50 µg/mL, and 100 µg/mL, respectively, compared to 5.8% in untreated cells. These results demonstrate that the methanolic extract of C. fruticosa leaf not only inhibits cellular proliferation but also actively promotes programmed cell death, a desirable mechanism in anticancer therapy.