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Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists01:18

Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists

Endothelins (ETs) are potent vasoactive peptides critical in the human body's various physiological and pathological processes. One of the most promising therapeutic strategies for treating pulmonary arterial hypertension (PAH) involves counteracting the effects of these endothelins using a class of drugs known as endothelin receptor antagonists.
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Updated: Jun 27, 2026

Preparation Of Neovascular Tissues from Human Glioma Tissues for Quantitative Proteomics Analysis of Tumor Angiogenesis
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Published on: March 20, 2026

Endothelin receptor B antagonists decrease glioma cell viability independently of their cognate receptor.

Jennifer P Montgomery1, Paul H Patterson

  • 1California Institute of Technology, 1200 E, California Blvd, MC 216-76, Pasadena, CA 91125, USA. jpmontgom@gmail.com

BMC Cancer
|December 2, 2008
PubMed
Summary
This summary is machine-generated.

Endothelin receptor type B (ETRB) antagonists reduce glioma and melanoma cell viability by activating DNA damage pathways, leading to cell cycle arrest and apoptosis. These effects are independent of ETRB inhibition.

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Predicting In Vivo Payloads Delivery using a Blood-brain Tumor-barrier in a Dish
13:34

Predicting In Vivo Payloads Delivery using a Blood-brain Tumor-barrier in a Dish

Published on: April 16, 2019

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Endothelin receptor antagonists show promise in cancer treatment, but their specific impact on glioma remains under-researched.
  • Glioma is a challenging cancer with limited effective therapeutic options.

Purpose of the Study:

  • To investigate the effects of endothelin receptor type B (ETRB)-specific antagonists on glioma and melanoma cell lines.
  • To elucidate the mechanisms underlying the observed effects of these antagonists on cancer cell viability and proliferation.

Main Methods:

  • Treatment of glioma (LN-229, SW1088) and melanoma (A375, WM35) cell lines with ETRB antagonists A-192621 and BQ788.
  • Assessment of cell viability, proliferation, and cell cycle distribution using flow cytometry and specific cell labeling techniques.
  • Gene expression analysis via microarray and RT-PCR, and evaluation of ETRB's role using small interfering RNA (siRNA).

Main Results:

  • ETRB antagonists A-192621 and BQ788 significantly reduced viable cell counts in both glioma and melanoma cell lines in a dose- and time-dependent manner.
  • A-192621 induced G2/M cell cycle arrest and apoptosis, and upregulated DNA damage-inducible genes.
  • The observed effects were independent of ETRB expression levels and ETRA antagonism.

Conclusions:

  • ETRB antagonists reduce glioma and melanoma cell viability through mechanisms independent of direct ETRB inhibition.
  • The primary mechanism involves the activation of stress and DNA damage response pathways, leading to cell cycle arrest and apoptosis.
  • This study provides novel evidence linking ETRB antagonist treatment to the induction of DNA damage response pathways in cancer cells.