Exploring the Phytochemical Composition of Bitter Melon Fruit and Molecular Responses to Its Extract in U87 MG Glioblastoma Cells
- 1Department of Biology, Gus R. Douglass Institute, West Virginia State University, Institute, WV 25112, USA
Abstract
Glioblastoma (GBM) is a highly aggressive type of brain cancer for which only a limited number of therapeutic options are available, highlighting the need to use multi-target strategies that interfere with the mechanisms by which the tumor survives and adapts to stress. In the present study, we investigated the antiproliferative and transcriptomic effects of bitter melon (Momordica charantia) extract (BME) in U87 MG glioblastoma cells. GC-MS analysis of bitter melon fruit revealed several bioactive metabolites known to have anticancer properties, including stigmasterol, β-sitosterol, caffeic acid, ferulic acid, and other fatty and organic acids, indicating that the extract has a chemically diverse composition that may explain its biological effects. BME markedly inhibited U87 MG cell proliferation in a dose- and time-dependent manner, with an IC50 of 659 µg/mL. Transcriptome analysis identified 908 differentially expressed genes, 380 upregulated and 528 downregulated. Functional and pathway analyses demonstrated enrichment in apoptosis, cellular senescence, ferroptosis, p53 signaling, and cellular stress responses, together with the suppression of PI3K–AKT, TNF, TGF-β, and cytokine–cytokine receptor signaling. The findings show that BME’s growth-inhibiting effect results from coordinated activation of cell-death and stress-response pathways along with reduced pro-tumor survival signaling. Combining metabolite profiling with transcriptomic analysis provides a molecular basis for identifying additional compounds in BME that are responsible for its antiproliferative action in glioblastoma and for verifying their effects.
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BibTeX
@article{reddy2026exploring,
title = {{Exploring the Phytochemical Composition of Bitter Melon Fruit and Molecular Responses to Its Extract in U87 MG Glioblastoma Cells}},
author = {Chinreddy Subramanyam Reddy and Dilip Nagisetty and Aishwarya Gaikwad and Nicole Tendayi Mashozhera and Virender Kumar and Gwonjin Lee and Robert T. Harris and Gerald R. Hankins and Umesh K. Reddy},
journal = {Molecules},
year = {2026},
month = oct,
doi = {10.3390/molecules31203714},
url = {https://www.mdpi.com/1420-3049/31/20/3714},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Exploring the Phytochemical Composition of Bitter Melon Fruit and Molecular Responses to Its Extract in U87 MG Glioblastoma Cells
AU - Chinreddy Subramanyam Reddy
AU - Dilip Nagisetty
AU - Aishwarya Gaikwad
AU - Nicole Tendayi Mashozhera
AU - Virender Kumar
AU - Gwonjin Lee
AU - Robert T. Harris
AU - Gerald R. Hankins
AU - Umesh K. Reddy
PY - 2026
DA - 2026/10/16
JO - Molecules
DO - 10.3390/molecules31203714
UR - https://www.mdpi.com/1420-3049/31/20/3714
AB - Glioblastoma (GBM) is a highly aggressive type of brain cancer for which only a limited number of therapeutic options are available, highlighting the need to use multi-target strategies that interfere with the mechanisms by which the tumor survives and adapts to stress. In the present study, we investigated the antiproliferative and transcriptomic effects of bitter melon (Momordica charantia) extract (BME) in U87 MG glioblastoma cells. GC-MS analysis of bitter melon fruit revealed several bioactive metabolites known to have anticancer properties, including stigmasterol, β-sitosterol, caffeic acid, ferulic acid, and other fatty and organic acids, indicating that the extract has a chemically diverse composition that may explain its biological effects. BME markedly inhibited U87 MG cell proliferation in a dose- and time-dependent manner, with an IC50 of 659 µg/mL. Transcriptome analysis identified 908 differentially expressed genes, 380 upregulated and 528 downregulated. Functional and pathway analyses demonstrated enrichment in apoptosis, cellular senescence, ferroptosis, p53 signaling, and cellular stress responses, together with the suppression of PI3K–AKT, TNF, TGF-β, and cytokine–cytokine receptor signaling. The findings show that BME’s growth-inhibiting effect results from coordinated activation of cell-death and stress-response pathways along with reduced pro-tumor survival signaling. Combining metabolite profiling with transcriptomic analysis provides a molecular basis for identifying additional compounds in BME that are responsible for its antiproliferative action in glioblastoma and for verifying their effects.
SN - 1420-3049
ER -