A characteristic feature of many cancer cells, including glioblastoma and ovarian carcinoma, is their reliance on exogenous methionine for tumor proliferation. L-methioninase, an enzyme that degrades methionine, is being investigated as a potential agent for specifically targeting methionine-dependent cancers by disrupting critical cellular pathways necessary for cancer cell survival. This study evaluated the cytotoxic effects of L-methioninase (L-Met) on the glioblastoma cell line A-172 and the ovarian carcinoma cell line SK-OV-3, focusing on cell survival, nuclear integrity, and metastatic potential.
L-Met was purified and tested for activity across a 25–200 µg/mL concentration range. Cytotoxicity was assessed using MTT assays, which measured viable cell count (VCC), total nuclear intensity (TNI), cell membrane permeability (CMP), and matrix metalloproteinase (MMP) activity. IC50 values were determined using Dunnett's multiple comparisons test.
L-Met significantly decreased cell viability in a dose-dependent manner for both cell lines. In A-172 cells, 200 and 100 µg/mL doses substantially reduced VCC and induced nuclear damage. In SK-OV-3 cells, these doses similarly reduced VCC and inhibited MMP activity, suggesting metastasis suppression. The IC50 values indicate that cancer cells are more sensitive to L-methioninase treatment than normal cells.
L-Met demonstrates significant cytotoxic effects against glioblastoma and ovarian cancer cells, primarily through the induction of DNA damage, disruption of cell membranes, and suppression of metastasis. These findings support the potential of L-Met as a therapeutic agent for methionine-dependent cancers.
Citation: Abbas Abed Noor Al-Owaidi, Mohammed Abdullah Jebor. Evaluation of L-methioninase as a targeted anticancer therapy in ovarian cancer and glioblastoma[J]. AIMS Biophysics, 2025, 12(2): 197-219. doi: 10.3934/biophy.2025012
A characteristic feature of many cancer cells, including glioblastoma and ovarian carcinoma, is their reliance on exogenous methionine for tumor proliferation. L-methioninase, an enzyme that degrades methionine, is being investigated as a potential agent for specifically targeting methionine-dependent cancers by disrupting critical cellular pathways necessary for cancer cell survival. This study evaluated the cytotoxic effects of L-methioninase (L-Met) on the glioblastoma cell line A-172 and the ovarian carcinoma cell line SK-OV-3, focusing on cell survival, nuclear integrity, and metastatic potential.
L-Met was purified and tested for activity across a 25–200 µg/mL concentration range. Cytotoxicity was assessed using MTT assays, which measured viable cell count (VCC), total nuclear intensity (TNI), cell membrane permeability (CMP), and matrix metalloproteinase (MMP) activity. IC50 values were determined using Dunnett's multiple comparisons test.
L-Met significantly decreased cell viability in a dose-dependent manner for both cell lines. In A-172 cells, 200 and 100 µg/mL doses substantially reduced VCC and induced nuclear damage. In SK-OV-3 cells, these doses similarly reduced VCC and inhibited MMP activity, suggesting metastasis suppression. The IC50 values indicate that cancer cells are more sensitive to L-methioninase treatment than normal cells.
L-Met demonstrates significant cytotoxic effects against glioblastoma and ovarian cancer cells, primarily through the induction of DNA damage, disruption of cell membranes, and suppression of metastasis. These findings support the potential of L-Met as a therapeutic agent for methionine-dependent cancers.
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Abbas Abed Noor Al-Owaidi, Mohammed Abdullah Jebor. Evaluation of L-methioninase as a targeted anticancer therapy in ovarian cancer and glioblastoma[J]. AIMS Biophysics, 2025, 12(2): 197-219. doi: 10.3934/biophy.2025012
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