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Role of ER in the Secretory Pathway01:17

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Eukaryotic cells have a special pathway that enables communication between various intracellular membrane-bound compartments and also with the extracellular environment. This pathway is termed as the secretory pathway.
Components of the secretory pathway
About a third of proteins synthesized in the cell are sorted via the secretory route. They shuffle between different compartments in membrane-bound vesicles until they reach their final destination. The main intracellular compartments involved...
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Export of Misfolded Proteins out of the ER01:32

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After folding, the ER assesses the quality of secretory and membrane proteins. The correctly folded proteins are cleared by the calnexin cycle for transport to their final destination, while misfolded proteins are held back in the ER lumen. The ER chaperones attempt to unfold and refold the misfolded proteins but sometimes fail to achieve the correct native conformation. Such terminally misfolded proteins are then exported to the cytosol by ER-associated degradation or ERAD pathway for...
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The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
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Tail-anchoring of Proteins in the ER Membrane01:45

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Tail-anchored, or TA, proteins are estimated to make up to 3-5% of membrane proteins found in the eukaryotic cell. Such proteins have a single transmembrane domain located approximately 30 amino acid residues upstream from the C-terminal end. As a result, the signal recognition particle (SRP) cannot guide a TA protein to the ER membrane for cotranslational insertion. Hence, they are integrated into the ER membrane post-translationally using their C-terminal end as the anchor. TA proteins...
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In the secretory pathway, vesicles transport proteins from one cellular compartment to another in forward transport to deliver the protein to its correct location. Occasionally, misfolded proteins and incorrect proteins escape their original compartments, and a retrieval pathway is used to return the escaped proteins to their original compartment.
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Inositol-requiring kinase one or IRE1 is the most conserved eukaryotic unfolded protein response (UPR) receptor. It is a type I transmembrane protein kinase receptor with a distinctive site-specific RNase activity. As the binding mechanics of the misfolded proteins with the N-terminal domain of IRE-1 are unclear, three binding models — direct, indirect, and allosteric -- are proposed for receptor activation. Nevertheless, it is known that once a misfolded protein associates with IRE1, it...
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Systems Biology of Metabolic Regulation by Estrogen Receptor Signaling in Breast Cancer
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El estrés del retículo endoplasmático inducido por ceramida como una vulnerabilidad objetivo en el cáncer de mama

Purab Pal1, Shweta Chitkara2, Godwin K Sarpey1

  • 1Department of Physiology and Biophysics, University of Illinois Chicago, IL, USA.

bioRxiv : the preprint server for biology
|September 2, 2025
PubMed
Resumen
Este resumen es generado por máquina.

La resistencia a la terapia endocrina en el cáncer de mama implica una reducción de las ceramidas y una mayor sensibilidad a la muerte celular inducida por la ceramida. Las ceramidas activan las vías de estrés del retículo endoplasmático (EnRS) a través de PERK, lo que lleva a la muerte celular en las células resistentes, particularmente a través de la interacción con TRAM1.

Palabras clave:
Ceramida y sus derivadosProteínas que interactúan con las ceramidasResistencia al tratamiento endocrinoEstrés en el retículo endoplasmáticoCáncer de mama luminalPerfectoTráfico de mercancías

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Área de la Ciencia:

  • En el campo de la oncología
  • Biología molecular
  • Biología celular

Sus antecedentes:

  • La terapia endocrina (ET) es efectiva para el cáncer de mama receptor de hormonas positivo, pero se enfrenta a desafíos con la resistencia al tratamiento y la recaída del paciente.
  • Las células de cáncer de mama resistentes a ET presentan un metabolismo alterado de la ceramida, mostrando niveles reducidos y una mayor sensibilidad a la muerte celular inducida por la ceramida.

Objetivo del estudio:

  • Investigar los mecanismos por los que las ceramidas inducen la muerte celular en las células de cáncer de mama resistentes a ET.
  • Identificar proteínas específicas involucradas en las vías de muerte celular mediadas por ceramida en la resistencia a ET.

Principales métodos:

  • Análisis de la reprogramación de la transcripción en las células resistentes a ET tras el tratamiento con ceramida.
  • Evaluación del papel del estrés del retículo endoplasmático (EnRS) y la vía PERK en la muerte celular inducida por ceramida.
  • Utilizando una sonda de ceramida fotoactivada para identificar las proteínas que interactúan con la ceramida (CIP).
  • Investigación de la función de TRAM1 en modelos de resistencia a ET y datos de pacientes.

Principales resultados:

  • Las ceramidas inducen una reprogramación transcripcional distinta en las células resistentes a ET, regulando al alza las vías de EnRS.
  • El EnRS inducido por ceramida depende de la vía PERK y media la muerte celular en múltiples modelos de resistencia a ET.
  • TRAM1 se identificó como una proteína clave que interactúa con las ceramidas (CIP) en las células resistentes a ET, asociada con una menor supervivencia libre de recaída y fenotipos agresivos de cáncer de mama.
  • La eliminación de TRAM1 imitaba los efectos de la ceramida en la resistencia a ET, destacando su papel en la muerte celular inducida por la ceramida.

Conclusiones:

  • Las células de cáncer de mama resistentes a ET son más sensibles al EnRS mediado por PERK en comparación con las células sensibles a ET.
  • Las ceramidas explotan esta sensibilidad al interactuar con CIP como TRAM1, activando PERK e induciendo la muerte celular preferentemente en modelos resistentes a ET.
  • La orientación hacia el eje ceramida-TRAM1-PERK presenta una estrategia terapéutica potencial para superar la resistencia de ET en el cáncer de mama.