JoVE - Journal of Visualized Experiments
JoVE Visualize
Contact Us
Esta página ha sido traducida por una máquina. Otras páginas pueden seguir apareciendo en inglés. View in English

El ligando Sas y su receptor PTP10D impulsan la competencia celular supresora del tumor.

  • 0Laboratory of Genetics, Graduate School of Biostudies, Kyoto University, Yoshida-Konoe-cho, Sakyo-ku, Kyoto 606-8501, Japan.
Nature +

|

17 de enero de 2017

|

17 de enero de 2017

Ver abstracta en PubMed

Resumen

Este resumen es generado por máquina.

Las células epiteliales normales eliminan a las vecinas oncogénicas mediante la competencia celular, mediada por el sistema Sas-PTP10D. Esta interacción restringe la señalización de EGFR, promoviendo la señalización de JNK para la supresión tumoral.

Área De La Ciencia

  • Biología del desarrollo
  • Biología celular
  • Investigación del cáncer

Sus Antecedentes

  • Las células epiteliales normales pueden suprimir el crecimiento tumoral a través de la competencia celular.
  • La pérdida de polaridad apico-basal en las células oncogénicas desencadena la eliminación por los vecinos de tipo salvaje.
  • El desencadenante molecular inicial para esta competencia de células supresoras de tumores sigue sin identificarse.

Objetivo Del Estudio

  • Para identificar las moléculas de la superficie celular que median la competencia celular supresora del tumor en Drosophila.
  • Para aclarar la vía de señalización iniciada en la interfaz entre las células normales y las deficientes de polaridad.

Principales Métodos

  • El cribado genético en el epitelio imaginario de Drosophila.
  • Análisis de las interacciones entre células y vías de señalización.
  • Investigando las funciones de las vías Sas, PTP10D, EGFR, JNK e Hippo.

Principales Resultados

  • El ligando Sas y el receptor PTP10D fueron identificados como mediadores clave de la competencia celular.
  • La señalización Sas-PTP10D en las células "perdedoras" restringe el EGFR, mejorando la eliminación mediada por JNK.
  • La ausencia de Sas-PTP10D conduce a la proliferación impulsada por el EGFR a través de la inactivación de la vía Hippo.

Conclusiones

  • Sas-PTP10D es el sistema de superficie celular crucial que reconoce y elimina las células oncogénicas con deficiencia de polaridad.
  • Este mecanismo pone de relieve cómo los epitélios normales suprimen activamente el desarrollo temprano del tumor.
  • Comprender esta vía ofrece información sobre la prevención del cáncer y las estrategias terapéuticas.

Videos de Conceptos Relacionados

Abnormal Proliferation 02:23

5.3K

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...

Receptor Downregulation in MVBs 01:15

2.9K

Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that  lead to cell proliferation, migration, and differentiation. Overexpression of EGFR  stimulates cells to proliferate. Excessive  EGFR...

Interactions Between Signaling Pathways 01:19

7.6K

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...

Amplifying Signals via Enzymatic Cascade 01:22

18.9K

When a ligand binds to a cell-surface receptor, the receptor's intracellular domain changes shape, which may either activate its enzyme function or allow its binding to other molecules. The initial signal is amplified by most signal transduction pathways. This means that a single ligand molecule can activate multiple molecules of a downstream target. Proteins that relay a signal are most commonly phosphorylated at one or more sites, activating or inactivating the protein. Kinases catalyze...

mTOR Signaling and Cancer Progression 03:03

5.0K

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...

Cancer-Critical Genes II: Tumor Suppressor Genes 01:05

10.0K

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...