Apigenin Induces Autophagy and Apoptosis in Chemoresistant Glioblastoma Cells and Inhibits Tumorigenicity Associated with Regulation of Immunomodulatory Proteins and Glial Cells Response.
Fuente:
PubMed
Saved in:
| Main Authors: | , , , , , , , , , , , , |
|---|---|
| Format: | Artículo científico |
| Language: | en |
| Published: |
Cells
2025
|
| Subjects: | |
| Online Access: | |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1868266141742268417 |
|---|---|
| author | Coelho, Paulo Lucas Cerqueira Santos, Cleonice Creusa Dos Silva, Alessandra Bispo da Silva, Karina Costa da Santana, Monique Reis de Santos, Balbino Lino Dos Lopes, Giselle Pinto de Faria Junier, Marie Pierre Chneiweiss, Hervé Moura-Neto, Vivaldo Costa, Maria de Fátima Dias Braga-de-Souza, Suzana Costa, Silvia Lima |
| author_facet | Coelho, Paulo Lucas Cerqueira Santos, Cleonice Creusa Dos Silva, Alessandra Bispo da Silva, Karina Costa da Santana, Monique Reis de Santos, Balbino Lino Dos Lopes, Giselle Pinto de Faria Junier, Marie Pierre Chneiweiss, Hervé Moura-Neto, Vivaldo Costa, Maria de Fátima Dias Braga-de-Souza, Suzana Costa, Silvia Lima Coelho, Paulo Lucas Cerqueira Santos, Cleonice Creusa Dos Silva, Alessandra Bispo da Silva, Karina Costa da Santana, Monique Reis de Santos, Balbino Lino Dos Lopes, Giselle Pinto de Faria Junier, Marie Pierre Chneiweiss, Hervé Moura-Neto, Vivaldo Costa, Maria de Fátima Dias Braga-de-Souza, Suzana Costa, Silvia Lima |
| collection | PubMed - marine biology |
| contents | Apigenin Induces Autophagy and Apoptosis in Chemoresistant Glioblastoma Cells and Inhibits Tumorigenicity Associated with Regulation of Immunomodulatory Proteins and Glial Cells Response. Coelho, Paulo Lucas Cerqueira Santos, Cleonice Creusa Dos Silva, Alessandra Bispo da Silva, Karina Costa da Santana, Monique Reis de Santos, Balbino Lino Dos Lopes, Giselle Pinto de Faria Junier, Marie Pierre Chneiweiss, Hervé Moura-Neto, Vivaldo Costa, Maria de Fátima Dias Braga-de-Souza, Suzana Costa, Silvia Lima Apigenin Glioblastoma Humans Animals Cell Line, Tumor Autophagy Apoptosis Drug Resistance, Neoplasm Rats Neuroglia Cell Survival Carcinogenesis Brain Neoplasms Cell Differentiation Cell Movement Glioblastomas (GBMs) are the most aggressive and common neoplasms that affect glial cells, presenting rapid growth, invasion, and resistance to treatments. Studies have demonstrated the potentially inhibitory effect of flavonoids on glioblastoma cells' stemness and viability. However, further research is needed to explore sensitivity and the mechanism of action in chemoresistant cells. In this study, we characterized the impact of apigenin treatment on the viability and differentiation of human GBM cells in vitro and its effects on tumorigenesis and regulation of the inflammatory response in vivo. The flavonoid apigenin reduced the viability of U-251 cells, patient-derived cells TG-1 and OB-1 stem cells in a dose-dependent manner, associated with the induction of acidic vesicle organelles formation and apoptosis. Treatment with apigenin also inhibited migration and induced neural differentiation in the remaining viable cells, characterized by a decrease in the expression of the precursor marker nestin and an increase in the expression of astrocyte and neuron markers, GFAP and β-III tubulin, respectively. The xenotransplantation of apigenin-pretreated U251 cells into rat brains did not lead to tumor formation, unlike untreated cells. The surrounding area of transplanted untreated U251 cells exhibited reactive microglia and astrocytes, along with increased VEGF expression, which was absent in implant sites of apigenin-pretreated GBM cells. Moreover, in this implant area, we observed a significant decrease in the expression of mRNA for inflammatory factors IL-1β, TNF, and NOS2, and the downregulation of IL-10 and IL-4. These results demonstrate that apigenin inhibits the growth of tumoral cells, affecting the viability of tumor stem cells and impairing tumorigenicity, while altering the regulatory profile of immunomodulatory proteins. Therefore, this flavonoid can be considered for further studies to determine its use as an adjuvant to the treatment of human GBMs. |
| format | Artículo científico |
| id | pubmed_41090780 |
| institution | PubMed |
| language | en |
| publishDate | 2025 |
| publisher | Cells |
| record_format | pubmed |
| spellingShingle | Apigenin Induces Autophagy and Apoptosis in Chemoresistant Glioblastoma Cells and Inhibits Tumorigenicity Associated with Regulation of Immunomodulatory Proteins and Glial Cells Response. Coelho, Paulo Lucas Cerqueira Santos, Cleonice Creusa Dos Silva, Alessandra Bispo da Silva, Karina Costa da Santana, Monique Reis de Santos, Balbino Lino Dos Lopes, Giselle Pinto de Faria Junier, Marie Pierre Chneiweiss, Hervé Moura-Neto, Vivaldo Costa, Maria de Fátima Dias Braga-de-Souza, Suzana Costa, Silvia Lima Apigenin Glioblastoma Humans Animals Cell Line, Tumor Autophagy Apoptosis Drug Resistance, Neoplasm Rats Neuroglia Cell Survival Carcinogenesis Brain Neoplasms Cell Differentiation Cell Movement Apigenin Induces Autophagy and Apoptosis in Chemoresistant Glioblastoma Cells and Inhibits Tumorigenicity Associated with Regulation of Immunomodulatory Proteins and Glial Cells Response. Coelho, Paulo Lucas Cerqueira Santos, Cleonice Creusa Dos Silva, Alessandra Bispo da Silva, Karina Costa da Santana, Monique Reis de Santos, Balbino Lino Dos Lopes, Giselle Pinto de Faria Junier, Marie Pierre Chneiweiss, Hervé Moura-Neto, Vivaldo Costa, Maria de Fátima Dias Braga-de-Souza, Suzana Costa, Silvia Lima Apigenin Glioblastoma Humans Animals Cell Line, Tumor Autophagy Apoptosis Drug Resistance, Neoplasm Rats Neuroglia Cell Survival Carcinogenesis Brain Neoplasms Cell Differentiation Cell Movement Glioblastomas (GBMs) are the most aggressive and common neoplasms that affect glial cells, presenting rapid growth, invasion, and resistance to treatments. Studies have demonstrated the potentially inhibitory effect of flavonoids on glioblastoma cells' stemness and viability. However, further research is needed to explore sensitivity and the mechanism of action in chemoresistant cells. In this study, we characterized the impact of apigenin treatment on the viability and differentiation of human GBM cells in vitro and its effects on tumorigenesis and regulation of the inflammatory response in vivo. The flavonoid apigenin reduced the viability of U-251 cells, patient-derived cells TG-1 and OB-1 stem cells in a dose-dependent manner, associated with the induction of acidic vesicle organelles formation and apoptosis. Treatment with apigenin also inhibited migration and induced neural differentiation in the remaining viable cells, characterized by a decrease in the expression of the precursor marker nestin and an increase in the expression of astrocyte and neuron markers, GFAP and β-III tubulin, respectively. The xenotransplantation of apigenin-pretreated U251 cells into rat brains did not lead to tumor formation, unlike untreated cells. The surrounding area of transplanted untreated U251 cells exhibited reactive microglia and astrocytes, along with increased VEGF expression, which was absent in implant sites of apigenin-pretreated GBM cells. Moreover, in this implant area, we observed a significant decrease in the expression of mRNA for inflammatory factors IL-1β, TNF, and NOS2, and the downregulation of IL-10 and IL-4. These results demonstrate that apigenin inhibits the growth of tumoral cells, affecting the viability of tumor stem cells and impairing tumorigenicity, while altering the regulatory profile of immunomodulatory proteins. Therefore, this flavonoid can be considered for further studies to determine its use as an adjuvant to the treatment of human GBMs. |
| title | Apigenin Induces Autophagy and Apoptosis in Chemoresistant Glioblastoma Cells and Inhibits Tumorigenicity Associated with Regulation of Immunomodulatory Proteins and Glial Cells Response. |
| topic | Apigenin Glioblastoma Humans Animals Cell Line, Tumor Autophagy Apoptosis Drug Resistance, Neoplasm Rats Neuroglia Cell Survival Carcinogenesis Brain Neoplasms Cell Differentiation Cell Movement |
| url | https://pubmed.ncbi.nlm.nih.gov/41090780/ |