Internalization-dependent regulation of HT29 cell proliferation by neurotensin.

Peptides

Institut de Pharmacologie Moléculaire et Cellulaire, Unité Mixte de Recherche 6097 du Centre National de la Recherche Scientifique, 660 route des Lucioles, Sophia Antipolis, 06560 Valbonne, France.

Published: October 2006

In this study, we have investigated the involvement of the internalization process induced by neurotensin (NT) on MAP kinases Erk1/2 activation, inositol phosphates (IP) accumulation and cell growth in the human colonic cancer cell line HT29. Reversible blocking of NT/neurotensin receptor (NTR) complex endocytosis by hyperosmolar sucrose totally abolished both the phosphorylation of the MAP kinases Erk1/2 and the [3H]-thymidine incorporation induced by the peptide. By contrast, NT-evoked IP formation was not affected by sucrose treatment. These results therefore indicate that NT/NTR complex endocytosis triggers MAP kinase activation and subsequently the growth of HT29 cells. This property could be useful for the development of novel anticancer treatments.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.peptides.2006.04.028DOI Listing

Publication Analysis

Top Keywords

map kinases
8
kinases erk1/2
8
complex endocytosis
8
internalization-dependent regulation
4
regulation ht29
4
ht29 cell
4
cell proliferation
4
proliferation neurotensin
4
neurotensin study
4
study investigated
4

Similar Publications

The ethanolic extract of Rhaphidophora peepla prevents inflammation by inhibiting the activation of Syk/AKT/NF-κB and TAK1/MAPK/AP-1.

Phytomedicine

January 2025

Department of Integrative Biotechnology, and Biomedical Institute for Convergence at SKKU, Sungkyunkwan University, Suwon 16419, Republic of Korea; Department of Biocosmetics, Sungkyunkwan University, Suwon 16419, Republic of Korea. Electronic address:

Background: Inflammation is the body's innate reaction to foreign pathogens and serves as a self-regulating mechanism. However, the immune system can mistakenly target the body's own tissues, triggering unnecessary inflammation. For millennia, medicinal plants have been employed for the treatment of diseases.

View Article and Find Full Text PDF

Studies have shown that uremia, renal failure and heart failure (HF) are closely related. However, whether this association reflects a causal effect is still unclear. The aim of this study was to evaluate the causal effect of uremic metabolites or toxins on HF.

View Article and Find Full Text PDF

Cadmium is a non-essential element and neurotoxin that causes neuroinflammation, which leads to neurodegenerative diseases and brain cancer. To date, there are no specific or effective therapeutic agents to control inflammation and alleviate cadmium-induced progressive destruction of brain cells. Fluoroquinolones (FQs), widely used antimicrobials with effective blood-brain barrier penetration, show promise in being repurposed as anti-inflammatory drugs.

View Article and Find Full Text PDF

Identities of functional pSer/Thr.Pro protein substrates of the PIN1 prolyl isomerase and its effects on downstream signaling in bladder carcinogenesis remain largely unknown. Phenotypically, we found that PIN1 positively regulated bladder cancer cell proliferation, cell motility and urothelium clearance capacity in vitro and controlled tumor growth and potential metastasis in vivo.

View Article and Find Full Text PDF

Low-grade gliomas and reactive piloid gliosis can present with overlapping features on conventional histology. Given the large implications for patient treatment, there is a need for effective methods to discriminate these morphologically similar but clinically distinct entities. Using routinely available stains, we hypothesize that a limited panel including SOX10, p16, and cyclin D1 may be useful in differentiating mitogen-activated protein (MAP) kinase-activated low-grade gliomas from piloid gliosis.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!