Wahyu Widowati
Faculty of Medicine, Maranatha Christian University, Bandung 40164, Indonesia

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Non-contact Electric Field Exposure Provides Potential Cancer Therapy through p53-Independent Proliferation Arrest and Intrinsic Pathway Apoptosis Induction in MG-63 Cell Lines Omat Rachmat Hasbullah; Ilma Fiddiyanti; Dewi Ratih Handayani; Endang Sutedja; Darmadji Ismono; Nucki Nursjamsi Hidajat; Wahyu Widowati; Ervi Afifah; Hanna Sari Widya Kusuma; Rizal Rizal; Firman Alamsyah; Warsito P. Taruno
HAYATI Journal of Biosciences Vol. 30 No. 3 (2023): May 2023
Publisher : Bogor Agricultural University, Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.4308/hjb.30.3.522-531

Abstract

Osteosarcoma is a highly malignant primary tumor on bone that mainly attacks children and young adolescents. Until now, osteosarcoma therapy still combines some high costs and invasive therapy modalities that may give side effects, such as pain and nausea. Our previous studies suggested that non-contact electric field has anti-proliferative effect on breast cancer cells, in vitro and in vivo. In this study, we were interested studying alternating current electric field effects on osteosarcoma cells progression as well as its potential cytotoxic effects. MG-63 human osteosarcoma cells were cultured and treated with 200 kHz for 6 days. Several genes of interest including p53, p21, MDM2, caspase-3, caspase-8, and caspase-9 were analyzed using real-time qPCR method. Apoptotic index was measured using flow-cytometry assay. Apoptosis was observed through p53-independent p21 pathway (p = 0.011). Cells undergoing apoptosis through internal pathways were shown by the increase of caspase-3 (p = 0.015) and caspase-9 (p = 0.001) levels, but not caspase-8 (p = 0.080). This treatment has successfully reduced the number of living osteosarcoma cells by 14.7% (p = 0.000) and increased cell death up to 4.26% (p = 0.055). Apoptotic index was markedly increased to 16% (p = 0.001). 200 kHz non-contact electric field exposure can disrupt osteosarcoma progression through disruption of normal cell cycle via p53-independent p21 pathway and induction of apoptosis.
Mangosteen Peel Extract (Garcinia mangostana L.) as a Potential Complementary of Leukemia Therapy: In Vitro and In Silico Studies Marisca Evalina Gondokesumo; Arina Novilla; Sijani Prahastuti; Fadhilah Haifa Zahiroh; Hanna Sari Widya Kusuma; Wahyu Widowati; Rizal Azis; Dhanar Septyawan Hadiprasetyo; Aris Muhammad Nurjamil; Wahyu Surakusumah; Khoerotul Nur Fadhilah Adha
Journal of Mathematical and Fundamental Sciences Vol. 57 No. 2 (2025)
Publisher : Directorate for Research and Innovation (DRI) ITB

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.5614/j.math.fund.sci.2025.57.2.3

Abstract

Leukemia is caused by abnormal white blood cell proliferation that leads to disruption of conventional blood cell functions. Mangosteen (Garcinia mangostana L.) contains phytochemical compounds with strong anticancer properties, according to various cancer studies. This study investigated the potential of mangosteen peel extract (MPE) as an anti-leukemia agent through molecular docking of LC-MS-identified compounds against FLT-1 and AKT proteins, followed by in vitro evaluation on HL-60 cells, namely cytotoxic (WST-8 assay), ROS levels and senescence (flow cytometry), and then FLT1 and AKT gene expression (qRT-PCR). LC-MS identified α-mangostin, β-mangostin, γ-mangostin, mangostinone, and epicatechin as the main compounds. Molecular docking revealed strong binding affinities from −8.5 to −9.9 kcal/mol against AKT, and from −9.0 to −9.9 kcal/mol against FLT-1. MPE (500 µg/mL) decreased cell viability and increased inhibition of HL-60 cells. Intracellular ROS levels decreased significantly at 0.6, 1.2, and 2.4 µg/mL MPE. MPE induced cell senescence especially at 1.2 and 2.4 µg/mL. Gene expression analysis revealed downregulation of AKT at 1.2 and 2.4 µg/mL and FLT1 at 2.4 µg/mL. These findings suggest that MPE may exert multifactorial anti-leukemic mechanisms, including apoptosis, ROS modulation, senescence induction, and regulation of AKT and FLT1 expression.