Dewi Ranggaini
Department Of Physiology, Division Of Oral Biology, Faculty Of Dentistry, Universitas Trisakti, Jl. Kyai Tapa No. 260, Jakarta 11440

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Journal : The Indonesian Biomedical Journal

Caffeic Acid Inhibits Tumour Mass Formation in MG-63 Cells-induced Nude Mice Ferry Sandra; Dewi Ranggaini; Laifa Annisa Hendarmin; Nurrani Mustika Dewi; Melanie Sadono Djamil
The Indonesian Biomedical Journal Vol 14, No 4 (2022)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v14i4.2078

Abstract

BACKGROUND: Formation of tumour mass is one symptom of osteosarcoma development. Caffeic acid has been known to provide effective treatment but has less side effect for some cancer therapy. Studies reported that caffeic acid might promote apoptosis in MG-63 osteosarcoma cells, however, the effect of caffeic acid treatment in preventing tumour mass formation has not been well elucidated, especially in MG-63 cells-induced nude mice in vivo.METHODS: MG-63 cells were pre-treated with 0, 1, or 10 µg/mL caffeic acid, and 6 hours after pre-treatment, MG-63 cells were injected into subcutaneous space of mice to induce osteosarcoma. Another model was also created by subcutaneously injecting MG-63 cells to the back of mice, and after 48 days, the visible tumour mass was injected intra-tumour with 0 or 10 µg/mL caffeic acid every 7 days for 6 times. After 90 days, mice were anaesthetised, and the nodule pictures were taken for observation and measurement. RESULTS: In pre-treated MG-63 cells-induced mice, volumes of the mass decreased in reverse with the dose of caffeic acid given. Ten µg/mL caffeic acid pre-treatment was able to significantly lower the mass volume compared to the untreated (p<0.05). Meanwhile, the intra-tumour treatment of 10 µg/mL caffeic acid, even though not significant, was able to inhibit tumour mass formation.CONCLUSION: Results of caffeic acid pre-treatment and caffeic acid treatment in tumour mass of mice show that caffeic acid is able to inhibit the MG-63 cells formation. This suggests that caffeic acid can be a potential anti-cancer agent.KEYWORDS: caffeic acid, osteosarcoma, MG-63 cells, tumour mass
Curcuma xanthorrhiza Rhizome Extract Induces Apoptosis in HONE-1 Nasopharyngeal Cancer Cells Through Bid Dewi Ranggaini; Ferry Sandra; Johni Halim; Solachuddin Jauhari Arief Ichwan; Melanie Sadono Djamil
The Indonesian Biomedical Journal Vol 15, No 1 (2023)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v15i1.2217

Abstract

BACKGROUND: Curcuma xanthorrhiza rhizomes have been demonstrated to have anticancer properties toward various types of cancer cells. The effect of C. xanthorrhiza rhizome extract (CXRE) on nasopharyngeal cancer (NPC) cells, including HONE-1 cell line has not been elucidated yet. Therefore, the effect of CXRE on the apoptosis of HONE-1 cells and its possible underlying mechanism are necessary to be explored.METHODS: C. xanthorrhiza rhizomes were minced, dried, extracted with distilled ethanol, filtered, and evaporated to produce CXRE. HONE-1 cells were seeded, starved, and treated with dimethyl sulfoxide (DMSO), Doxorubicin, or various concentrations of CXRE. Treated HONE-1 cells were stained with 4',6'-diamidino-2-phenylindole (DAPI) and the number of viable cells was counted. HONE-1 cells were also collected, lysed, and further processed for immunoblotting analysis to measure Bid activity.RESULTS: The number of viable HONE-1 cells decreased in concentration- and time-dependent manner. The number of viable cells in 50 and 250 μg/mL CXRE-treated groups were significantly lower compared with that in the DMSO-treated group after 24 h. At 48 h incubation period, the number of viable cells in 10, 50 and 250 μg/mL CXRE-treated groups were significantly lower compared with that in the DMSO-treated group. The number of viable cells in 250 μg/mL CXRE-treatment group was not significantly different compared with that in the Doxorubicin-treated group after 48 h. Bid expression levels in CXRE-treated groups were lower compared with that in the DMSO-treated group.CONCLUSION: CXRE could induce apoptosis via Bid activation, hence reducing the viability of HONE-1 cells.KEYWORDS: Curcuma xanthorrhiza, nasopharyngeal cancer, HONE-1 cells, apoptosis, Bid
Elephantopus scaber Linn. Leaf Extract Sensitizes Doxorubicin in Inducing Apoptosis in HSC-3 Tongue Cancer Cells through Inhibiting Survivin Activity at Thr34 Ferry Sandra; Ria Aryani Hayuningtyas; Dewi Ranggaini; Tiffany Pang; Alifah Evi Scania; Kyung Hoon Lee
The Indonesian Biomedical Journal Vol 16, No 4 (2024)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v16i4.3096

Abstract

BACKGROUND: Previous research has demonstrated the effect of Elephantopus scaber Linn. leaf extract (ESLE) on various cancer cell lines. However, research on the effects of ESLE on oral squamous cell carcinoma (OSCC), especially tongue cancer, is still lacking. Moreover, the apoptotic mechanisms induced by ESLE are not well understood and require further exploration. Therefore, this study was conducted to investigate the effects of ESLE on cell viability and apoptosis in human squamous cell carcinoma (HSC)-3 tongue cancer cells.METHODS: HSC-3 cells were treated with varying concentrations of ESLE, doxorubicin, and a combination of both. Cell viability and apoptosis were assessed using MTT and Sub-G1 assays. The expression levels of survivin and its phosphorylated form at threonine (Thr)34 were evaluated using Western blot analysis.RESULTS: ESLE exhibited a concentration-dependent cytotoxic effect on HSC-3 cells in decreasing cell viability (Kruskal Wallis, p=0.001) and increasing apoptotic cells (ANOVA, p=0.001) significantly. When combined with doxorubicin, ESLE further enhanced the induction of apoptosis compared with doxorubicin alone. The combined treatment resulted in a decrease in the levels of phosphorylated survivin (p-Surv) Thr34, indicating the inhibition of survivin's anti-apoptotic function.CONCLUSION: ESLE significantly enhances the efficacy of doxorubicin, thereby sensitizing its ability to induce apoptosis in HSC-3 tongue cancer cells. This sensitization occurs through the inhibition of survivin activity, particularly at the Thr34 phosphorylation site. These findings suggest that ESLE could serve as a potential adjuvant to improve the effectiveness of doxorubicin in inducing apoptosis in tongue cancer cells.KEYWORDS: Elephantopus scaber, doxorubicin, tongue cancer, HSC-3 cells, apoptosis, Survivin, Thr34 phosphorylation