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Updated: Jan 31, 2026

Establishment of Cancer Stem Cell Cultures from Human Conventional Osteosarcoma
Published on: October 14, 2016
Indole-3-Carbinol Induces Apoptosis in Human Osteosarcoma MG-63 and U2OS Cells
Chang Min Lee1, Jongsung Lee2, Myeong Jin Nam1
1Department of Life Science, Gachon University, Seongnam 13120, Republic of Korea.
Abstract:
This study was focused on investigating the anticancer potential of indole-3-carbinol (I3C) against osteosarcoma MG-63 and U2OS cells. A wound healing assay indicated that IC3 inhibited migration of MG-63 and U2OS cells. MTT, WST-1, and colony formation assays revealed that treatment of MG-63 and U2OS cells with I3C decreased cell viability. Fluorescence-activated cell sorting (FACS) analysis showed that I3C induced apoptosis in a dose- and time-dependent manner in MG-63 and U2OS cells. Moreover, via terminal deoxynucleotidyl transferase- (TdT-) mediated dUTP-biotin nick-end labeling (TUNEL) assay, we detected that I3C induced DNA fragmentation. Western blotting demonstrated that activated forms of caspase-3, caspase-7, and caspase-9, as well as poly (ADP-ribose) polymerase (PARP) were increased in MG-63 and U2OS cells, following treatment with I3C. Furthermore, protein expression levels of FOXO3, Bax, and Bim extra-large form were increased while those of Akt, JNK, p38, phosphorylated ERK, and Bcl-xL were decreased by I3C treatment in MG-63 and U2OS cells. Thus, the study indicates that I3C may induce apoptosis in human osteosarcoma MG-63 and U2OS cells via the activation of apoptotic signaling pathways by FOXO3.
Insights
Indole-3-carbinol (I3C) shows anticancer potential by inhibiting osteosarcoma cell migration and viability. I3C induces apoptosis through DNA fragmentation and activation of key apoptotic signaling pathways, including FOXO3.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Osteosarcoma is a primary bone cancer with limited treatment options.
- Indole-3-carbinol (I3C), a compound found in cruciferous vegetables, has demonstrated potential anticancer properties.
- Investigating novel therapeutic agents for osteosarcoma is crucial for improving patient outcomes.
Purpose of the Study:
- To investigate the anticancer effects of indole-3-carbinol (I3C) on human osteosarcoma cell lines (MG-63 and U2OS).
- To elucidate the mechanisms underlying I3C-induced cell death in osteosarcoma.
Main Methods:
- Cell viability was assessed using MTT, WST-1, and colony formation assays.
- Cell migration was evaluated using a wound healing assay.
- Apoptosis induction was analyzed by fluorescence-activated cell sorting (FACS) and terminal deoxynucleotidyl transferase- (TdT-) mediated dUTP-biotin nick-end labeling (TUNEL) assay.
- Western blotting was employed to examine the expression of apoptosis-related proteins (caspases, PARP, FOXO3, Bax, Bim, Akt, JNK, p38, ERK, Bcl-xL).
Main Results:
- I3C significantly inhibited the migration and decreased the viability of MG-63 and U2OS osteosarcoma cells.
- I3C treatment induced apoptosis and DNA fragmentation in a dose- and time-dependent manner.
- I3C upregulated pro-apoptotic proteins (activated caspases-3, -7, -9, PARP, FOXO3, Bax, Bim) and downregulated anti-apoptotic proteins (Akt, JNK, p38, p-ERK, Bcl-xL).
- FOXO3 activation was identified as a key mediator in I3C-induced apoptosis.
Conclusions:
- Indole-3-carbinol (I3C) exhibits significant anticancer potential against human osteosarcoma cells.
- I3C effectively induces apoptosis through the activation of intrinsic apoptotic pathways, involving FOXO3, caspases, and modulation of Bcl-2 family proteins.
- I3C represents a promising therapeutic candidate for osteosarcoma treatment, warranting further investigation.
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