Video Experimental Relacionado

Updated: Sep 9, 2025

Co-immunoprecipitation Assay Using Endogenous Nuclear Proteins from Cells Cultured Under Hypoxic Conditions

Co-immunoprecipitation Assay Using Endogenous Nuclear Proteins from Cells Cultured Under Hypoxic Conditions

Published on: August 2, 2018

VIPR1 induce la cuproptosis e inhibe la vía HIF-1α en el cáncer de colon

Xue Liu¹, Ye Lin¹, Jingzhi Zhang¹

¹Department of Gastroenterology, The Affiliated Ganzhou Hospital of Nanchang University, Ganzhou City, Jiangxi Province, China.

Journal of biochemical and molecular toxicology

|September 3, 2025

Resumen

La cuproptosis, una vía de muerte celular programada, actúa como un supresor de tumores en el cáncer de colon. La sobreexpresión del gen VIPR1 promueve la cuproposis, inhibiendo el crecimiento y la migración de las células cancerosas mediante la regulación a la baja de la señalización HIF- 1α.

Área de la Ciencia:

En el campo de la oncología
Investigación de la muerte celular
Biología molecular

Sus antecedentes:

La cuproptosis, una nueva muerte celular programada, está implicada en la progresión del tumor, pero su papel en el cáncer de colon no está claro.
Comprender los genes relacionados con la cuproposis es crucial para desarrollar diagnósticos y terapias para el cáncer de colon.

Objetivo del estudio:

Investigar el papel de los genes relacionados con la cuproposis en el desarrollo y la progresión del cáncer de colon.
Identificar posibles biomarcadores de diagnóstico y objetivos terapéuticos dentro de las vías de cuproposis.

Principales métodos:

Análisis bioinformático de conjuntos de datos de cáncer de colon (GSE4183, GSE74602) para identificar genes relacionados con la cuproposis expresados diferencialmente.
Experimentos in vitro con líneas celulares de cáncer de colon (HT29, HCT116) para evaluar la proliferación, la migración y la invasión.
Ensayos funcionales que evalúan la función mitocondrial, la reprogramación metabólica y el papel del factor 1 alfa inducible por hipoxia (HIF-1α).
Quelación del cobre (TTM) y activación de la señalización VIPR1 (VIP) para confirmar la dependencia de la cuproptosis y el potencial terapéutico.

Principales resultados:

Se identificaron cinco genes hub relacionados con la cuproposis regulados hacia abajo (VIPR1, PYY, NPY, VIP, SST) como posibles biomarcadores del cáncer de colon.
La sobreexpresión de VIPR1 suprimió la proliferación, migración e invasión de las células de cáncer de colon, aumentando la regulación de FDX1 y DLST.
Los efectos supresores de tumores de VIPR1 dependían de la cuproptosis y estaban mediados por la inhibición de la señalización de HIF- 1α.
El tratamiento con agonistas de VIPR1 inhibió aún más el comportamiento de las células cancerosas y reguló a la baja el HIF- 1α.

Conclusiones:

VIPR1 funciona como supresor tumoral en el cáncer de colon al mejorar la cuproposis y alterar la aptitud metabólica a través de la inhibición de HIF- 1α.
VIPR1 representa un objetivo terapéutico prometedor para la intervención del cáncer de colon.
Los genes relacionados con la cuproptosis tienen un potencial significativo como biomarcadores de diagnóstico para el cáncer de colon.

Palabras clave:

Vía HIF-1α Se incluyen los siguientes elementos:Los biomarcadores Cáncer de colon Cuerpo de los niños

Más Videos Relacionados

A Murine Cell Line Based Model of Chronic CDK9 Inhibition to Study Widespread Non-Genetic Transcriptional Elongation Defects TEdeff in Cancers

A Murine Cell Line Based Model of Chronic CDK9 Inhibition to Study Widespread Non-Genetic Transcriptional Elongation Defects TEdeff in Cancers

Published on: September 26, 2019

Ex Vivo Treatment Response of Primary Tumors and/or Associated Metastases for Preclinical and Clinical Development of Therapeutics

Ex Vivo Treatment Response of Primary Tumors and/or Associated Metastases for Preclinical and Clinical Development of Therapeutics

Published on: October 2, 2014

Videos de Conceptos Relacionados

PI3K/mTOR/AKT Signaling Pathway

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast, mTORC2 consists of a...

Regulation of Angiogenesis and Blood Supply

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits. Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...

The Intrinsic Apoptotic Pathway

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...

Inhibition of Cdk Activity

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...

Cancer-Critical Genes II: Tumor Suppressor Genes

Cancer-Critical Genes II: Tumor Suppressor Genes

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...

Abnormal Proliferation

Abnormal Proliferation

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...