Fossils discovered in mountain range

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A team of Spanish researchers has discovered fossils of Ordovician conodonts dating to between 446 and 444 million years ago for the first time in the western Mediterranean. The discovery of these very primitive marine vertebrates has helped scientists to reconstruct the palaeogeography of the Cordillera Bética mountain range.

Their study shows that the mountain system in the south of the Iberian Peninsula was located alongside the Alps at that time.

In 2006, a group of Andalusian geologists found the oldest fossils in the Cordillera Bética, dating from the late Ordovician period between 446 and 444 million years ago, in the Maláguide Complex in Ardales (Malaga). This was also the first solid evidence of Ordovician rocks in the Bética range.

The researchers analysed the characteristics of the conodont remains they found, the presence of certain species, and the absence of others, and compared these with others of a similar age found in the macizo ibérico (essentially the western half of the Iberian Peninsula) and other ranges in the area.

The results of the study show that, during the late Ordovician period, the Maláguide Complex was not to be found with the rest of the Iberian Peninsula along the edge of the palaeo-continent of Gondwana, «but was rather at a much lower latitude much closer to the Alps, with its Ordovician conodont fauna showing much closer similarities to the fauna of this area,»  said Rosario Rodríguez-Cañero, lead author of the study at the Department of Stratigraphy and Palaeontology of the University of Granada.

The conodonts were small, eel-shaped animals without any vertebral column, which measured a few tenths of a millimetre in length, and inhabited the seas during the Palaeozoic era and became extinct at the end of the Triassic (around 205 million years ago).

The findings have been published in the latest issue of the journal Terra Nova.

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Oldest fossils discovered in Cordillera Betica mountain range

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A team of Spanish researchers has discovered fossils of Ordovician conodonts dating to between 446 and 444 million years ago for the first time in the western Mediterranean.

The discovery of these very primitive marine vertebrates has helped scientists to reconstruct the palaeogeography of the Cordillera Bética mountain range.

Their study shows that the mountain system in the south of the Iberian Peninsula was located alongside the Alps at that time.

In 2006, a group of Andalusian geologists found the oldest fossils in the Cordillera Bética, dating from the late Ordovician period between 446 and 444 million years ago, in the Malaguide Complex in Ardales
(Malaga). This was also the first solid evidence of Ordovician rocks in the Bética range.

The researchers analysed the characteristics of the conodont remains they found, the presence of certain species, and the absence of others, and compared these with others of a similar age found in the macizo ibérico (essentially the western half of the Iberian Peninsula) and other ranges in the area.

The results of the study show that, during the late Ordovician period, the Malaguide Complex was not to be found with the rest of the Iberian Peninsula along the edge of the palaeo-continent of Gondwana, «but was rather at a much lower latitude much closer to the Alps, with its Ordovician conodont fauna showing much closer similarities to the fauna of this area,» said Rosario Rodriguez-Cañero, lead author of the study at the Department of Stratigraphy and Palaeontology of the University of Granada.

The conodonts were small, eel-shaped animals without any vertebral column, which measured a few tenths of a millimetre in length, and inhabited the seas during the Palaeozoic era and became extinct at the end of the Triassic (around 205 million years ago).

The findings have been published in the latest issue of the journal Terra Nova

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Oldest fossils discovered in Cordillera Betica mountain range

Escrito por

A team of Spanish researchers has discovered fossils of Ordovician conodonts dating to between 446 and 444 million years ago for the first time in the western Mediterranean.

The discovery of these very primitive marine vertebrates has helped scientists to reconstruct the palaeogeography of the Cordillera Betica mountain range.

Their study shows that the mountain system in the south of the Iberian Peninsula was located alongside the Alps at that time.

In 2006, a group of Andalusian geologists found the oldest fossils in the Cordillera Betica, dating from the late Ordovician period between 446 and 444 million years ago, in the Mal guide Complex in Ardales (Malaga). This was also the first solid evidence of Ordovician rocks in the Betica range.

The researchers analysed the characteristics of the conodont remains they found, the presence of certain species, and the absence of others, and compared these with others of a similar age found in the macizo iberico (essentially the western half of the Iberian Peninsula) and other ranges in the area.

The results of the study show that, during the late Ordovician period, the Mal guide Complex was not to be found with the rest of the Iberian Peninsula along the edge of the palaeo-continent of Gondwana, «but was rather at a much lower latitude much closer to the Alps, with its Ordovician conodont fauna showing much closer similarities to the fauna of this area,» said Rosario Rodr¡guez-Ca¤ero, lead author of the study at the Department of Stratigraphy and Palaeontology of the University of Granada.

The conodonts were small, eel-shaped animals without any vertebral column, which measured a few tenths of a millimetre in length, and inhabited the seas during the Palaeozoic era and became extinct at the end of the Triassic (around 205 million years ago).

The findings have been published in the latest issue of the journal Terra Nova.

Descargar

Oldest fossils discovered in Cordillera Betica mountain range

Escrito por

A team of Spanish researchers has discovered fossils of Ordovician conodonts dating to between 446 and 444 million years ago for the first time in the western Mediterranean.

The discovery of these very primitive marine vertebrates has helped scientists to reconstruct the palaeogeography of the Cordillera Betica mountain range.

Their study shows that the mountain system in the south of the Iberian Peninsula was located alongside the Alps at that time.

In 2006, a group of Andalusian geologists found the oldest fossils in the Cordillera Betica, dating from the late Ordovician period between 446 and 444 million years ago, in the Mal guide Complex in Ardales (Malaga). This was also the first solid evidence of Ordovician rocks in the Betica range.

The researchers analysed the characteristics of the conodont remains they found, the presence of certain species, and the absence of others, and compared these with others of a similar age found in the macizo iberico (essentially the western half of the Iberian Peninsula) and other ranges in the area.

The results of the study show that, during the late Ordovician period, the Mal guide Complex was not to be found with the rest of the Iberian Peninsula along the edge of the palaeo-continent of Gondwana, «but was rather at a much lower latitude much closer to the Alps, with its Ordovician conodont fauna showing much closer similarities to the fauna of this area,» said Rosario Rodr¡guez-Ca¤ero, lead author of the study at the Department of Stratigraphy and Palaeontology of the University of Granada.

The conodonts were small, eel-shaped animals without any vertebral column, which measured a few tenths of a millimetre in length, and inhabited the seas during the Palaeozoic era and became extinct at the end of the Triassic (around 205 million years ago).

The findings have been published in the latest issue of the journal Terra Nova.

Descargar

A Protein Called cFLIP Makes Tumor Cells in Breast Cancer Resistant to Treatments

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Researchers at the Andalusian Institute for Molecular Biology and Regenerative Medicine (CABIMER) and the University of Granada found that cFLIP -an inhibitor of death ligand-induced apoptosis- is not only essential in breast tumor cells resistance to TRAIL treatments (a death ligand with a potent therapeutic potential against cancer), but this protein is also key to the survival of such cancer cells.

Researchers proved that a variation in the expression of this protein may lead to the normal development of breast epithelium. This is an important finding to be considered in the design of cFLIP-targeted therapies against cancer.

This finding might very useful for scientists, that could design cancer therapies aimed at interfering the action of this protein. Such was the conclusion drawn by the researchers at the Andalusian Institute for Molecular Biology and Regenerative Medicine (CABIMER), in collaboration with the University of Granada.

The research conducted by Rosario Yerbes Cadenas, PhD candidate at the University of Granada, was led by professor Abelardo López Rivas, of CABIMER, and was aimed at analysing the potential of cFLIP inhibitors in cancer therapies.

At present, TRAIL is a death-ligand of the TNF family, with significant therapeutic potential against cancer, basically due to its ability to induce apoptosis in cancer cells without displaying significant toxicity toward normal cells. However, there are tumor cells that are resistant to TRAIL-induced apoptosis for unknown causes.

This study analysed the role of cFLIP in breast cancer cells’ resistance to TRAIL-induced apoptosis. Thus, researchers concluded that cFLIP is key in these cells’ resistance to TRAIL. Such conclusion was drawn from the evidence that the inhibition of their expression through treatments with Doxorubicin (anthracycline, widely used in chemotherapy) or with SAHA (Histone deacetylases inhibitor), as well as the silencing of its expression through cFLIP siRNA oligos (small interfering RNA), resulted in the sensitisation of breast cancer cells to TRAIL-induced apoptosis.

The authors of this research proved that cFLIP plays a survival role in tumorous and non-tumorous breast epithelial cells, since the inhibition of its expression induces apoptosis. This type of apoptosis requires the formation of the death-inducing signalling complex, which includes TRAIL-R2 receptor, adapter molecule FADD and procaspase-8- but is TRAIL-independent itself.

Conversely, in the light of the cFLIP relevance in controlling apoptosis, researchers studied the role of cFLIP in breast epithelial cells MCF-10A morphogenesis -a process where apoptosis plays an essential role. Thus, cFLIPL/cFLIPS overexpression inhibits lumen formation in acini from breast epithelial cells when they are cultured in a 3D extracellular matrix (3D cultures). Additionally, inhibition of cFLIP expression prevents the development of acini, since cells with low expression of cFLIP are unfeasible.

For this reason, regulation of cFLIP expression was very relevant to this research. Scientists determined that the PI3K/AKT signalling pathway is not the main responsible for cFLIP synthesis in breast cancer cell, but may be it is NF-kB pathway.

Additionally, this study revealed that the ubiquitin-proteasome system plays a key role in cFLIP cell degradation. At present, researchers are trying to identify E3-ubiquitin ligase protein, responsible for cFLIP degradation by such system.

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Ideal

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Pág. 14: La idea de declarar BIC la Vega toma fuerza entre asociaciones y colectivos nacionales

Pág. 24: La UGR limita a 50 personas los servicios mínimos durante las fiestas de Navidad

La Habana y Granada comparten sus tesis

Pág. 25: ‘Honoris Causa’ para el decano de Educación

Pág. 61: Nuevo tomo de teatro de Mira Amescua

Marta Madrid expone desde hoy sus ilustraciones en el Carmen de la Victoria

Descarga por URL: http://canal.ugr.es/medios-impresos/item/download/37603

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A protein called cFLIP makes tumor cells in breast cancer resistant to treatments

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Researchers at the Andalusian Institute for Molecular Biology and Regenerative Medicine (CABIMER) and the University of Granada found that cFLIP -an inhibitor of death ligand-induced apoptosis- is not only essential in breast tumor cells resistance to TRAIL treatments (a death ligand with a potent therapeutic potential against cancer), but this protein is also key to the survival of such cancer cells.

Researchers proved that a variation in the expression of this protein may lead to the normal development of breast epithelium. This is an important finding to be considered in the design of cFLIP-targeted therapies against cancer.

The research conducted by Rosario Yerbes Cadenas, PhD candidate at the University of Granada, was led by professor Abelardo López Rivas, of CABIMER, and was aimed at analysing the potential of cFLIP inhibitors in cancer therapies.

At present, TRAIL is a death-ligand of the TNF family, with significant therapeutic potential against cancer, basically due to its ability to induce apoptosis in cancer cells without displaying significant toxicity toward normal cells. However, there are tumor cells that are resistant to TRAIL-induced apoptosis for unknown causes.

A Key Component

This study analysed the role of cFLIP in breast cancer cells’ resistance to TRAIL-induced apoptosis. Thus, researchers concluded that cFLIP is key in these cells’ resistance to TRAIL. Such conclusion was drawn from the evidence that the inhibition of their expression through treatments with Doxorubicin (anthracycline, widely used in chemotherapy) or with SAHA (Histone deacetylases inhibitor), as well as the silencing of its expression through cFLIP siRNA oligos (small interfering RNA), resulted in the sensitisation of breast cancer cells to TRAIL-induced apoptosis.

The authors of this research proved that cFLIP plays a survival role in tumorous and non-tumorous breast epithelial cells, since the inhibition of its expression induces apoptosis. This type of apoptosis requires the formation of the death-inducing signalling complex, which includes TRAIL-R2 receptor, adapter molecule FADD and procaspase-8- but is TRAIL-independent itself.

Conversely, in the light of the cFLIP relevance in controlling apoptosis, researchers studied the role of cFLIP in breast epithelial cells MCF-10A morphogenesis -a process where apoptosis plays an essential role. Thus, cFLIPL/cFLIPS overexpression inhibits lumen formation in acini from breast epithelial cells when they are cultured in a 3D extracellular matrix (3D cultures). Additionally, inhibition of cFLIP expression prevents the development of acini, since cells with low expression of cFLIP are unfeasible.

For this reason, regulation of cFLIP expression was very relevant to this research. Scientists determined that the PI3K/AKT signalling pathway is not the main responsible for cFLIP synthesis in breast cancer cell, but may be it is NF-kB pathway.

Additionally, this study revealed that the ubiquitin-proteasome system plays a key role in cFLIP cell degradation. At present, researchers are trying to identify E3-ubiquitin ligase protein, responsible for cFLIP degradation by such system.

More information:
References:

Flavopiridol induces cFLIP degradation by the proteasome and promotes TRAIL-induced early signal transduction and apoptosis in breast tumor cells. Carmen Palacios, Rosario Yerbes and Abelardo López-Rivas. Cancer Research, 2006

Roscovitine sensitizes breast cancer cells to TRAIL-induced apoptosis through a pleiotropic mechanism. Ortiz-Ferrón G, Yerbes R, Eramo A, López-Pérez AI, De Maria R, López-Rivas A. Cell Research, 2008

Cellular cFLIPL plays a survival role and regulates morphogenensis in breast epithelial cells. Yerbes R., Palacios C, Reginato MJ. and López-Rivas A. The Journal of Biological Chemistry (en revisión).

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A protein called cFLIP makes tumor cells in breast cancer resistant to treatments

Escrito por

Researchers at the Andalusian Institute for Molecular Biology and Regenerative Medicine (CABIMER) and the University of Granada found that cFLIP –an inhibitor of death ligand-induced apoptosis– is not only essential in breast tumor cells resistance to TRAIL treatments (a death ligand with a potent therapeutic potential against cancer), but this protein is also key to the survival of such cancer cells. Researchers proved that a variation in the expression of this protein may lead to the normal development of breast epithelium. This is an important finding to be considered in the design of cFLIP-targeted therapies against cancer.

The research conducted by Rosario Yerbes Cadenas, PhD candidate at the University of Granada, was led by professor Abelardo López Rivas, of CABIMER, and was aimed at analysing the potential of cFLIP inhibitors in cancer therapies.

At present, TRAIL is a death-ligand of the TNF family, with significant therapeutic potential against cancer, basically due to its ability to induce apoptosis in cancer cells without displaying significant toxicity toward normal cells. However, there are tumor cells that are resistant to TRAIL-induced apoptosis for unknown causes.

A Key Component

This study analysed the role of cFLIP in breast cancer cells’ resistance to TRAIL-induced apoptosis. Thus, researchers concluded that cFLIP is key in these cells’ resistance to TRAIL. Such conclusion was drawn from the evidence that the inhibition of their expression through treatments with Doxorubicin (anthracycline, widely used in chemotherapy) or with SAHA (Histone deacetylases inhibitor), as well as the silencing of its expression through cFLIP siRNA oligos (small interfering RNA), resulted in the sensitisation of breast cancer cells to TRAIL-induced apoptosis.

The authors of this research proved that cFLIP plays a survival role in tumorous and non-tumorous breast epithelial cells, since the inhibition of its expression induces apoptosis. This type of apoptosis requires the formation of the death-inducing signalling complex, which includes TRAIL-R2 receptor, adapter molecule FADD and procaspase-8- but is TRAIL-independent itself.

Conversely, in the light of the cFLIP relevance in controlling apoptosis, researchers studied the role of cFLIP in breast epithelial cells MCF-10A morphogenesis -a process where apoptosis plays an essential role. Thus, cFLIPL/cFLIPS overexpression inhibits lumen formation in acini from breast epithelial cells when they are cultured in a 3D extracellular matrix (3D cultures). Additionally, inhibition of cFLIP expression prevents the development of acini, since cells with low expression of cFLIP are unfeasible.

For this reason, regulation of cFLIP expression was very relevant to this research. Scientists determined that the PI3K/AKT signalling pathway is not the main responsible for cFLIP synthesis in breast cancer cell, but may be it is NF-kB pathway.

Additionally, this study revealed that the ubiquitin-proteasome system plays a key role in cFLIP cell degradation. At present, researchers are trying to identify E3-ubiquitin ligase protein, responsible for cFLIP degradation by such system.

Descargar

A protein called cFLIP makes tumor cells in breast cancer resistant to treatments

Escrito por

Researchers at the Andalusian Institute for Molecular Biology and Regenerative Medicine (CABIMER) and the University of Granada found that cFLIP –an inhibitor of death ligand-induced apoptosis– is not only essential in breast tumor cells resistance to TRAIL treatments (a death ligand with a potent therapeutic potential against cancer), but this protein is also key to the survival of such cancer cells.

Researchers proved that a variation in the expression of this protein may lead to the normal development of breast epithelium. This is an important finding to be considered in the design of cFLIP-targeted therapies against cancer.

The research conducted by Rosario Yerbes Cadenas, PhD candidate at the University of Granada, was led by professor Abelardo López Rivas, of CABIMER, and was aimed at analysing the potential of cFLIP inhibitors in cancer therapies.

At present, TRAIL is a death-ligand of the TNF family, with significant therapeutic potential against cancer, basically due to its ability to induce apoptosis in cancer cells without displaying significant toxicity toward normal cells. However, there are tumor cells that are resistant to TRAIL-induced apoptosis for unknown causes.

A Key Component

This study analysed the role of cFLIP in breast cancer cells’ resistance to TRAIL-induced apoptosis. Thus, researchers concluded that cFLIP is key in these cells’ resistance to TRAIL. Such conclusion was drawn from the evidence that the inhibition of their expression through treatments with Doxorubicin (anthracycline, widely used in chemotherapy) or with SAHA (Histone deacetylases inhibitor), as well as the silencing of its expression through cFLIP siRNA oligos (small interfering RNA), resulted in the sensitisation of breast cancer cells to TRAIL-induced apoptosis.

The authors of this research proved that cFLIP plays a survival role in tumorous and non-tumorous breast epithelial cells, since the inhibition of its expression induces apoptosis. This type of apoptosis requires the formation of the death-inducing signalling complex, which includes TRAIL-R2 receptor, adapter molecule FADD and procaspase-8- but is TRAIL-independent itself.

Conversely, in the light of the cFLIP relevance in controlling apoptosis, researchers studied the role of cFLIP in breast epithelial cells MCF-10A morphogenesis -a process where apoptosis plays an essential role. Thus, cFLIPL/cFLIPS overexpression inhibits lumen formation in acini from breast epithelial cells when they are cultured in a 3D extracellular matrix (3D cultures). Additionally, inhibition of cFLIP expression prevents the development of acini, since cells with low expression of cFLIP are unfeasible.

For this reason, regulation of cFLIP expression was very relevant to this research. Scientists determined that the PI3K/AKT signalling pathway is not the main responsible for cFLIP synthesis in breast cancer cell, but may be it is NF-kB pathway.

Additionally, this study revealed that the ubiquitin-proteasome system plays a key role in cFLIP cell degradation. At present, researchers are trying to identify E3-ubiquitin ligase protein, responsible for cFLIP degradation by such system.

Descargar

A Protein Called CFLIP Makes Tumor Cells In Breast Cancer Resistant To Treatments

Escrito por

Researchers at the Andalusian Institute for Molecular Biology and Regenerative Medicine (CABIMER) and the University of Granada found that cFLIP –an inhibitor of death ligand-induced apoptosis– is not only essential in breast tumor cells resistance to TRAIL treatments (a death ligand with a potent therapeutic potential against cancer), but this protein is also key to the survival of such cancer cells.

Researchers proved that a variation in the expression of this protein may lead to the normal development of breast epithelium. This is an important finding to be considered in the design of cFLIP-targeted therapies against cancer.

The research conducted by Rosario Yerbes Cadenas, PhD candidate at the University of Granada, was led by professor Abelardo López Rivas, of CABIMER, and was aimed at analysing the potential of cFLIP inhibitors in cancer therapies.

At present, TRAIL is a death-ligand of the TNF family, with significant therapeutic potential against cancer, basically due to its ability to induce apoptosis in cancer cells without displaying significant toxicity toward normal cells. However, there are tumor cells that are resistant to TRAIL-induced apoptosis for unknown causes.

A Key Component

This study analysed the role of cFLIP in breast cancer cells’ resistance to TRAIL-induced apoptosis. Thus, researchers concluded that cFLIP is key in these cells’ resistance to TRAIL. Such conclusion was drawn from the evidence that the inhibition of their expression through treatments with Doxorubicin (anthracycline, widely used in chemotherapy) or with SAHA (Histone deacetylases inhibitor), as well as the silencing of its expression through cFLIP siRNA oligos (small interfering RNA), resulted in the sensitisation of breast cancer cells to TRAIL-induced apoptosis.

The authors of this research proved that cFLIP plays a survival role in tumorous and non-tumorous breast epithelial cells, since the inhibition of its expression induces apoptosis. This type of apoptosis requires the formation of the death-inducing signalling complex, which includes TRAIL-R2 receptor, adapter molecule FADD and procaspase-8- but is TRAIL-independent itself.

Conversely, in the light of the cFLIP relevance in controlling apoptosis, researchers studied the role of cFLIP in breast epithelial cells MCF-10A morphogenesis -a process where apoptosis plays an essential role. Thus, cFLIPL/cFLIPS overexpression inhibits lumen formation in acini from breast epithelial cells when they are cultured in a 3D extracellular matrix (3D cultures). Additionally, inhibition of cFLIP expression prevents the development of acini, since cells with low expression of cFLIP are unfeasible.

For this reason, regulation of cFLIP expression was very relevant to this research. Scientists determined that the PI3K/AKT signalling pathway is not the main responsible for cFLIP synthesis in breast cancer cell, but may be it is NF-kB pathway.

Additionally, this study revealed that the ubiquitin-proteasome system plays a key role in cFLIP cell degradation. At present, researchers are trying to identify E3-ubiquitin ligase protein, responsible for cFLIP degradation by such system.

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Granada Hoy

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Pág. 25: Catorce cubanos se doctoran gracias a la colaboración entre la UGR y La Habana

Pág. 33: Una investigación de la Universidad avala la calidad del agua de la Vega

Pág. 35: Jornadas El PTS, eje de un congreso

Pág. 60: Una exposición refleja los procesos de creación de la lectura

La UGR edita el tomo X del Teatro Completo de Mira de Amescua

Contraportada: Gustavo Cobreiro. Rector Universidad de La Habana

Descarga por URL: http://canal.ugr.es/medios-impresos/item/download/37598

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Study reports role of cFLIP in breast cancer cells’ resistance to TRAIL-induced apoptosis

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This finding might very useful for scientists, that could design cancer therapies aimed at interfering the action of this protein. Such was the conclusion drawn by the researchers at the Andalusian Institute for Molecular Biology and Regenerative Medicine (CABIMER), in collaboration with the University of Granada.

Researchers at the Andalusian Institute for Molecular Biology and Regenerative Medicine (CABIMER) and the University of Granada found that cFLIP -an inhibitor of death ligand-induced apoptosis- is not only essential in breast tumor cells resistance to TRAIL treatments (a death ligand with a potent therapeutic potential against cancer), but this protein is also key to the survival of such cancer cells.

Researchers proved that a variation in the expression of this protein may lead to the normal development of breast epithelium. This is an important finding to be considered in the design of cFLIP-targeted therapies against cancer.

The research conducted by Rosario Yerbes Cadenas, PhD candidate at the University of Granada, was led by professor Abelardo López Rivas, of CABIMER, and was aimed at analysing the potential of cFLIP inhibitors in cancer therapies.

At present, TRAIL is a death-ligand of the TNF family, with significant therapeutic potential against cancer, basically due to its ability to induce apoptosis in cancer cells without displaying significant toxicity toward normal cells. However, there are tumor cells that are resistant to TRAIL-induced apoptosis for unknown causes.

A Key Component

This study analysed the role of cFLIP in breast cancer cells’ resistance to TRAIL-induced apoptosis. Thus, researchers concluded that cFLIP is key in these cells’ resistance to TRAIL. Such conclusion was drawn from the evidence that the inhibition of their expression through treatments with Doxorubicin (anthracycline, widely used in chemotherapy) or with SAHA (Histone deacetylases inhibitor), as well as the silencing of its expression through cFLIP siRNA oligos (small interfering RNA), resulted in the sensitisation of breast cancer cells to TRAIL-induced apoptosis.

The authors of this research proved that cFLIP plays a survival role in tumorous and non-tumorous breast epithelial cells, since the inhibition of its expression induces apoptosis. This type of apoptosis requires the formation of the death-inducing signalling complex, which includes TRAIL-R2 receptor, adapter molecule FADD and procaspase-8- but is TRAIL-independent itself.

Conversely, in the light of the cFLIP relevance in controlling apoptosis, researchers studied the role of cFLIP in breast epithelial cells MCF-10A morphogenesis -a process where apoptosis plays an essential role. Thus, cFLIPL/cFLIPS overexpression inhibits lumen formation in acini from breast epithelial cells when they are cultured in a 3D extracellular matrix (3D cultures). Additionally, inhibition of cFLIP expression prevents the development of acini, since cells with low expression of cFLIP are unfeasible.

For this reason, regulation of cFLIP expression was very relevant to this research. Scientists determined that the PI3K/AKT signalling pathway is not the main responsible for cFLIP synthesis in breast cancer cell, but may be it is NF-kB pathway.

Additionally, this study revealed that the ubiquitin-proteasome system plays a key role in cFLIP cell degradation. At present, researchers are trying to identify E3-ubiquitin ligase protein, responsible for cFLIP degradation by such system.

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