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Abstract
Discussion Forum (0)
Poster Category: Research and Education
AACP Section: Biological Sciences
Objectives: Glioblastomas are typified by their aggressive invasive characteristics. Surgical debulking of the tumor, radiotherapy, and the use of alkylating agents such as temozolomide are currently used to treat glioblastoma. There is a need for the development of newer agents to combat this deadly tumor. N-Substituted imidooxy compounds were synthesized and screened for in vitro cytotoxicity in glioblastoma cell lines. These imidooxy compounds (E49, E38, and KL-1) were originally reported to have anticonvulsant properties in small mammals.
We aimed to evaluate the in vitro biological activity and signaling mechanisms affected by these compounds for their potential anticancer activity and determine their effects on glioblastoma cell proliferation and apoptosis
Methods: The viability potentials of the imidooxy compounds were tested using (3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide (MTT), cell counts, and wound healing assays. The effects of these imidooxy compounds on glioma cells were further validated using lactate dehydrogenase (LDH) and colony formation assays. In addition, we investigated the survival and apoptotic molecular signaling targets perturbed by these newly synthesized compounds using Western blot analysis and flow cytometry.
Results: Our results show that there was a time-and-concentration-dependent reduction in cell viability and inhibition of wound healing in the cells tested. Western blot analyses of the gene expression data revealed genes such as mTOR/Akt/NF kappa B to be associated with imidooxy sensitivity. E49, E38, and KL-1 treatment induced apoptosis by cleaving PARP, activating caspases, and downregulating BCL-xL. Based on these results, E49, E38, and KL-1 suppressed cell growth and induced apoptosis in glioblastoma cell lines.
Conclusion: Our data provide in vitro support for the anticancer activity of the imidooxy compounds (E49, E38, and KL-1) in glioma cells by downregulating cancer survival proteins.
AACP Section: Biological Sciences
Objectives: Glioblastomas are typified by their aggressive invasive characteristics. Surgical debulking of the tumor, radiotherapy, and the use of alkylating agents such as temozolomide are currently used to treat glioblastoma. There is a need for the development of newer agents to combat this deadly tumor. N-Substituted imidooxy compounds were synthesized and screened for in vitro cytotoxicity in glioblastoma cell lines. These imidooxy compounds (E49, E38, and KL-1) were originally reported to have anticonvulsant properties in small mammals.
We aimed to evaluate the in vitro biological activity and signaling mechanisms affected by these compounds for their potential anticancer activity and determine their effects on glioblastoma cell proliferation and apoptosis
Methods: The viability potentials of the imidooxy compounds were tested using (3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide (MTT), cell counts, and wound healing assays. The effects of these imidooxy compounds on glioma cells were further validated using lactate dehydrogenase (LDH) and colony formation assays. In addition, we investigated the survival and apoptotic molecular signaling targets perturbed by these newly synthesized compounds using Western blot analysis and flow cytometry.
Results: Our results show that there was a time-and-concentration-dependent reduction in cell viability and inhibition of wound healing in the cells tested. Western blot analyses of the gene expression data revealed genes such as mTOR/Akt/NF kappa B to be associated with imidooxy sensitivity. E49, E38, and KL-1 treatment induced apoptosis by cleaving PARP, activating caspases, and downregulating BCL-xL. Based on these results, E49, E38, and KL-1 suppressed cell growth and induced apoptosis in glioblastoma cell lines.
Conclusion: Our data provide in vitro support for the anticancer activity of the imidooxy compounds (E49, E38, and KL-1) in glioma cells by downregulating cancer survival proteins.
Poster Category: Research and Education
AACP Section: Biological Sciences
Objectives: Glioblastomas are typified by their aggressive invasive characteristics. Surgical debulking of the tumor, radiotherapy, and the use of alkylating agents such as temozolomide are currently used to treat glioblastoma. There is a need for the development of newer agents to combat this deadly tumor. N-Substituted imidooxy compounds were synthesized and screened for in vitro cytotoxicity in glioblastoma cell lines. These imidooxy compounds (E49, E38, and KL-1) were originally reported to have anticonvulsant properties in small mammals.
We aimed to evaluate the in vitro biological activity and signaling mechanisms affected by these compounds for their potential anticancer activity and determine their effects on glioblastoma cell proliferation and apoptosis
Methods: The viability potentials of the imidooxy compounds were tested using (3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide (MTT), cell counts, and wound healing assays. The effects of these imidooxy compounds on glioma cells were further validated using lactate dehydrogenase (LDH) and colony formation assays. In addition, we investigated the survival and apoptotic molecular signaling targets perturbed by these newly synthesized compounds using Western blot analysis and flow cytometry.
Results: Our results show that there was a time-and-concentration-dependent reduction in cell viability and inhibition of wound healing in the cells tested. Western blot analyses of the gene expression data revealed genes such as mTOR/Akt/NF kappa B to be associated with imidooxy sensitivity. E49, E38, and KL-1 treatment induced apoptosis by cleaving PARP, activating caspases, and downregulating BCL-xL. Based on these results, E49, E38, and KL-1 suppressed cell growth and induced apoptosis in glioblastoma cell lines.
Conclusion: Our data provide in vitro support for the anticancer activity of the imidooxy compounds (E49, E38, and KL-1) in glioma cells by downregulating cancer survival proteins.
AACP Section: Biological Sciences
Objectives: Glioblastomas are typified by their aggressive invasive characteristics. Surgical debulking of the tumor, radiotherapy, and the use of alkylating agents such as temozolomide are currently used to treat glioblastoma. There is a need for the development of newer agents to combat this deadly tumor. N-Substituted imidooxy compounds were synthesized and screened for in vitro cytotoxicity in glioblastoma cell lines. These imidooxy compounds (E49, E38, and KL-1) were originally reported to have anticonvulsant properties in small mammals.
We aimed to evaluate the in vitro biological activity and signaling mechanisms affected by these compounds for their potential anticancer activity and determine their effects on glioblastoma cell proliferation and apoptosis
Methods: The viability potentials of the imidooxy compounds were tested using (3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide (MTT), cell counts, and wound healing assays. The effects of these imidooxy compounds on glioma cells were further validated using lactate dehydrogenase (LDH) and colony formation assays. In addition, we investigated the survival and apoptotic molecular signaling targets perturbed by these newly synthesized compounds using Western blot analysis and flow cytometry.
Results: Our results show that there was a time-and-concentration-dependent reduction in cell viability and inhibition of wound healing in the cells tested. Western blot analyses of the gene expression data revealed genes such as mTOR/Akt/NF kappa B to be associated with imidooxy sensitivity. E49, E38, and KL-1 treatment induced apoptosis by cleaving PARP, activating caspases, and downregulating BCL-xL. Based on these results, E49, E38, and KL-1 suppressed cell growth and induced apoptosis in glioblastoma cell lines.
Conclusion: Our data provide in vitro support for the anticancer activity of the imidooxy compounds (E49, E38, and KL-1) in glioma cells by downregulating cancer survival proteins.
In Vitro Inhibition of Glioblastoma Cell Growth by N-Substituted Imidooxy Compounds
Samson Amos
Abstract
Discussion Forum (0)
Poster Category: Research and Education
AACP Section: Biological Sciences
Objectives: Glioblastomas are typified by their aggressive invasive characteristics. Surgical debulking of the tumor, radiotherapy, and the use of alkylating agents such as temozolomide are currently used to treat glioblastoma. There is a need for the development of newer agents to combat this deadly tumor. N-Substituted imidooxy compounds were synthesized and screened for in vitro cytotoxicity in glioblastoma cell lines. These imidooxy compounds (E49, E38, and KL-1) were originally reported to have anticonvulsant properties in small mammals.
We aimed to evaluate the in vitro biological activity and signaling mechanisms affected by these compounds for their potential anticancer activity and determine their effects on glioblastoma cell proliferation and apoptosis
Methods: The viability potentials of the imidooxy compounds were tested using (3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide (MTT), cell counts, and wound healing assays. The effects of these imidooxy compounds on glioma cells were further validated using lactate dehydrogenase (LDH) and colony formation assays. In addition, we investigated the survival and apoptotic molecular signaling targets perturbed by these newly synthesized compounds using Western blot analysis and flow cytometry.
Results: Our results show that there was a time-and-concentration-dependent reduction in cell viability and inhibition of wound healing in the cells tested. Western blot analyses of the gene expression data revealed genes such as mTOR/Akt/NF kappa B to be associated with imidooxy sensitivity. E49, E38, and KL-1 treatment induced apoptosis by cleaving PARP, activating caspases, and downregulating BCL-xL. Based on these results, E49, E38, and KL-1 suppressed cell growth and induced apoptosis in glioblastoma cell lines.
Conclusion: Our data provide in vitro support for the anticancer activity of the imidooxy compounds (E49, E38, and KL-1) in glioma cells by downregulating cancer survival proteins.
AACP Section: Biological Sciences
Objectives: Glioblastomas are typified by their aggressive invasive characteristics. Surgical debulking of the tumor, radiotherapy, and the use of alkylating agents such as temozolomide are currently used to treat glioblastoma. There is a need for the development of newer agents to combat this deadly tumor. N-Substituted imidooxy compounds were synthesized and screened for in vitro cytotoxicity in glioblastoma cell lines. These imidooxy compounds (E49, E38, and KL-1) were originally reported to have anticonvulsant properties in small mammals.
We aimed to evaluate the in vitro biological activity and signaling mechanisms affected by these compounds for their potential anticancer activity and determine their effects on glioblastoma cell proliferation and apoptosis
Methods: The viability potentials of the imidooxy compounds were tested using (3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide (MTT), cell counts, and wound healing assays. The effects of these imidooxy compounds on glioma cells were further validated using lactate dehydrogenase (LDH) and colony formation assays. In addition, we investigated the survival and apoptotic molecular signaling targets perturbed by these newly synthesized compounds using Western blot analysis and flow cytometry.
Results: Our results show that there was a time-and-concentration-dependent reduction in cell viability and inhibition of wound healing in the cells tested. Western blot analyses of the gene expression data revealed genes such as mTOR/Akt/NF kappa B to be associated with imidooxy sensitivity. E49, E38, and KL-1 treatment induced apoptosis by cleaving PARP, activating caspases, and downregulating BCL-xL. Based on these results, E49, E38, and KL-1 suppressed cell growth and induced apoptosis in glioblastoma cell lines.
Conclusion: Our data provide in vitro support for the anticancer activity of the imidooxy compounds (E49, E38, and KL-1) in glioma cells by downregulating cancer survival proteins.
Poster Category: Research and Education
AACP Section: Biological Sciences
Objectives: Glioblastomas are typified by their aggressive invasive characteristics. Surgical debulking of the tumor, radiotherapy, and the use of alkylating agents such as temozolomide are currently used to treat glioblastoma. There is a need for the development of newer agents to combat this deadly tumor. N-Substituted imidooxy compounds were synthesized and screened for in vitro cytotoxicity in glioblastoma cell lines. These imidooxy compounds (E49, E38, and KL-1) were originally reported to have anticonvulsant properties in small mammals.
We aimed to evaluate the in vitro biological activity and signaling mechanisms affected by these compounds for their potential anticancer activity and determine their effects on glioblastoma cell proliferation and apoptosis
Methods: The viability potentials of the imidooxy compounds were tested using (3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide (MTT), cell counts, and wound healing assays. The effects of these imidooxy compounds on glioma cells were further validated using lactate dehydrogenase (LDH) and colony formation assays. In addition, we investigated the survival and apoptotic molecular signaling targets perturbed by these newly synthesized compounds using Western blot analysis and flow cytometry.
Results: Our results show that there was a time-and-concentration-dependent reduction in cell viability and inhibition of wound healing in the cells tested. Western blot analyses of the gene expression data revealed genes such as mTOR/Akt/NF kappa B to be associated with imidooxy sensitivity. E49, E38, and KL-1 treatment induced apoptosis by cleaving PARP, activating caspases, and downregulating BCL-xL. Based on these results, E49, E38, and KL-1 suppressed cell growth and induced apoptosis in glioblastoma cell lines.
Conclusion: Our data provide in vitro support for the anticancer activity of the imidooxy compounds (E49, E38, and KL-1) in glioma cells by downregulating cancer survival proteins.
AACP Section: Biological Sciences
Objectives: Glioblastomas are typified by their aggressive invasive characteristics. Surgical debulking of the tumor, radiotherapy, and the use of alkylating agents such as temozolomide are currently used to treat glioblastoma. There is a need for the development of newer agents to combat this deadly tumor. N-Substituted imidooxy compounds were synthesized and screened for in vitro cytotoxicity in glioblastoma cell lines. These imidooxy compounds (E49, E38, and KL-1) were originally reported to have anticonvulsant properties in small mammals.
We aimed to evaluate the in vitro biological activity and signaling mechanisms affected by these compounds for their potential anticancer activity and determine their effects on glioblastoma cell proliferation and apoptosis
Methods: The viability potentials of the imidooxy compounds were tested using (3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide (MTT), cell counts, and wound healing assays. The effects of these imidooxy compounds on glioma cells were further validated using lactate dehydrogenase (LDH) and colony formation assays. In addition, we investigated the survival and apoptotic molecular signaling targets perturbed by these newly synthesized compounds using Western blot analysis and flow cytometry.
Results: Our results show that there was a time-and-concentration-dependent reduction in cell viability and inhibition of wound healing in the cells tested. Western blot analyses of the gene expression data revealed genes such as mTOR/Akt/NF kappa B to be associated with imidooxy sensitivity. E49, E38, and KL-1 treatment induced apoptosis by cleaving PARP, activating caspases, and downregulating BCL-xL. Based on these results, E49, E38, and KL-1 suppressed cell growth and induced apoptosis in glioblastoma cell lines.
Conclusion: Our data provide in vitro support for the anticancer activity of the imidooxy compounds (E49, E38, and KL-1) in glioma cells by downregulating cancer survival proteins.
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