Cervical and breast cancers are two of the most common cancer affecting women. In Indonesia, there are 65,858 cases of breast cancer and 36,633 cases of cervical cancer have been recorded. Chemotherapy, using agents such as cisplatin and doxorubicin, is one of the main cancer therapies and works by targeting cancer cells. However, this therapy lacks selectivity and damages normal cells, leading to adverse side effects. An alternative chemopreventive treatment is Myricetin, a compound predicted to potentially target VEGF, a critical factor in angiogenesis, making it a promising anticancer agent. This study aims to evaluate the safety of Myricetin on Vero cells (normal cells), assess its anticancer activity on T47D and HeLa cells, and predict its mechanism of action. The anticancer activity was evaluated using the Microculture Tetrazolium Technique (MTT) assay on HeLa, T47D, and Vero cells. VEGF receptors were identified through a Network Pharmacology approach. The study also involved the Molecular Docking of Myricetin, cisplatin, and doxorubicin compounds with the 5DXH receptor. The results showed that Myricetin exhibited high cytotoxic activity against HeLa and T47D cells, with IC50 values of 22.70 μg/mL and 51.43 μg/mL, respectively, while demonstrating significantly lower cytotoxicity against Vero cells, with a CC50 value of 1445.2 μg/mL. In comparison, the CC50 values for cisplatin and doxorubicin against Vero cells were 6.53 μg/mL and 13.76 μg/mL, respectively, indicating that Myricetin is considerably less toxic to normal cells. Myricetin's Selectivity Index (SI) was 63.64 for HeLa cells and 28.09 for T47D cells, demonstrating superior selectivity compared to cisplatin and doxorubicin. These findings suggest that Myricetin has promising anticancer potential with a better safety profile than conventional chemotherapeutic agents.

Objective: Eleutherine palmifolia (L.) Merr. extract (EPE) containing isoliquiritigenin and oxyresveratrol is believed to be an anticancer agent. This study evaluates colon histopathology, TNF-α, TGF-β, and hepatotoxicity on BALB/c mice colitis-associated colon cancer (CAC) model treated with EPE. Methods: In vivo study was performed on BALB/c mice CAC model induced by 10 mg/kgBW AOM on the first day followed by administration that each cycle consisted of 5% DSS in water for seven days and regular water for seven days. The indicators of the formation of CAC were observed by a fecal occult blood test (FOBT) and serum amyloid α (SAA) test. The treatment was conducted once a week started from the seventh week up to the twentieth week with six treatment groups: I was administrated by regular water only (negative control), II was administrated by AOM and DSS only (positive control), III was administrated by doxorubicin, IV-VI were treated by EPE (0.25 mg/kg BW, 0.50 mg/kg BW, and 1.00 mg/kg BW) respectively. The colon and liver’s histopathology was observed using hematoxylin-eosin (HE) staining, TNF-α with immunohistochemistry (IHC), and level measurement of TGF-β colon with ELISA reader. The data were used one-way ANOVA followed by post hoc as statistical analysis. Results: The administration of EPE increased the expression of TNF-α, the total of goblet cells of the colon, and decreased the level of TGF-β. Administration of EPE 0.50 mg/20g BW decreased a liver histopathological score but induced a histopathological alteration of the liver at a dose of 1.00 mg/20g BW. Conclusion: This study indicate that EPE could be recommended as a colon anticancer through increase the goblet cells, induce apoptosis through increase TNF-α, and decrease TGF-β.

Antimalarial study using methanol extract and ethyl acetate fraction of sunflower leaves had been done. The study was conducted to know antimalarial activity between methanol extract and ethyl acetate fraction at Plasmodium falciparum parasites 3D7 strain. Separation of compounds was done by maceration using methanol and partition using ethyl acetate. Identification of ethyl acetate fraction was done by using UPLC-MS instrument. The results shown ethyl acetate fraction obtained the highest peak based on database were artemisinin, heliangolide, linolenic acid, linoleic acid eupalinolide C. The results of antimalarial study shown that methanol extract had IC₅₀ 22.18 mg/mL, and ethyl acetate fraction had IC₅₀ 16.68 mg/mL. Antimalarial activity between methanol extract and ethyl acetate fraction showed no significant difference.

Eleutherine palmifolia (L.) Merr. is a typical plant found in Central Kalimantan that has been used empirically by the Dayak people as medicine for various diseases, including cancer. The plant contains flavonoid compounds that potentially used as an anticancer. The purpose of this study is to find the most active fraction, indicated by its cytotoxic potency on HeLa cervical cancer cell line, and to identify compounds in E. palmifolia bulbs fraction. E. palmifolia bulbs was extracted by maceration. The extraction with ultrasonic bath and partition fractionation was conducted by using n-hexane, chloroform, and ethyl acetate. Each fraction was tested for toxicity level on HeLa cells using MTT assay. The identification of active compounds was carried out by Ultra Performance Liquid Chromatography-Mass Spectrometry (UPLC-MS). The result showed that based on the IC50 value, the ethyl acetate fraction had the highest bioactivity. IC50 values of n-hexane, chloroform, and ethyl acetate fractions were 250.77±19.01; 720.46±42.38; and 44.34±9.45μg/mL, respectively. The identification of the active compound in ethyl acetate fraction resulted 28 chemical compounds. Compounds with the highest percentage area were isoliquiritigenin and oxyresveratrol. The ethyl acetate fraction of E. palmifolia bulbs is potential to be developed as an anticancer candidate (phytopharmaceutical). Keywords: Compound identification, Anticancer activity, Eleutherine palmifolia (L.) Merr., cervical cancer

Eleutherine palmifolia (L.) Merr. (E. palmifolia) is an Indonesian native plant that has the potential to be developed into phytopharmaca. The differences in growth locations are thought to cause variation in the content of metabolite compounds which affect differences in pharmacological activity. This study aims to determine the profile of metabolites E. palmifolia bulb from several regions in Indonesia. The samples were collected from six different locations, namely East Java, Central Java, West Java, East Borneo, Central Borneo, and South Borneo. Sample extraction was carried out using Ultrasonic Assisted Extraction (UAE) method with 96% ethanol. The analysis of the content of metabolites was carried out using UPLC-QTOF-MS/MS with a stationary phase column C₁₈ (Okta Decyl Silica), mobile phase mixture of formic acid /water 0.1/99.9 (v/v), and formic acid/acetonitrile 0,1/99,9 (v/v). The results of the analysis were interpreted using software Masslynx and continued with chemometric analysis using the method Principle Component Analysis (PCA). The results showed that there were differences in the content of the metabolite compounds in E. palmifolia bulb originating from six different regions.

Objective: The objective of this study was to evaluate the potential and mechanisms of phytochemicals in Eleutherine bulbosa (EBE) in inducing apoptosis and inhibiting the cell cycle in breast cancer through a network pharmacology approach and in vitro validation. Methods: This research employed a literature review approach to identify active anti-cancer compounds and utilized a network pharmacology approach to predict the mechanisms of action of EBE compounds in breast cancer. In addition, in vitro experiments were conducted using MTT method to evaluate the effects of EBE on the cytotoxicity of T47D cells, and the flow cytometry method was employed to determine the impact of EBE on apoptosis and the cell cycle. Results: The network pharmacology analysis revealed that EBE had an impact on 42 genes involved in breast cancer, including 23 important target genes implicated in the pathophysiology of breast cancer. Pathway analysis using the KEGG database showed a close association between EBE and crucial signaling pathways in breast cancer, including P53 signaling pathway, MAPK signaling pathway, PI3K-Akt signaling pathway, apoptosis and cell cycle. In vitro experiments demonstrated that EBE exhibited moderate anti-cancer activity. Furthermore, EBE demonstrated significant potential in inducing apoptosis in breast cancer cells, with a percentage of apoptotic cells reaching 93.6%. Additionally, EBE was observed to disrupt the cell cycle, leading to a significant increase in the sub G1 and S phases, and a significant decrease in the G2-M and G1 phases. Conclusion: EBE has the potential to be an anti-cancer agent through various mechanisms, including apoptosis induction and cell cycle inhibition in breast cancer cells. These findings provide new insights into the potential of EBE as an alternative treatment for breast cancer.