Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Activation of protein kinase G is sufficient to induce apoptosis and inhibit cell migration in colon cancer cells.

Cancer research - 1 Jun 2004

Deguchi Atsuko, Thompson W Joseph, Weinstein I Bernard

Abstract excerpt

The activation of protein kinase G (PKG) by cGMP has become of considerable interest as a novel molecular mechanism for the induction of apoptosis in cancer cells, because sulindac sulfone (exisulind, Aptosyn) and certain derivatives that inhibit cGMP-phosphodiesterases and thereby increase cellular levels of cGMP appear to induce apoptosis via this mechanism. However, other effects of these compounds have not...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Cell Division
Share to Cell Movement
Share to Colonic Neoplasms

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cyclic GMP-Dependent Protein Kinases

Share to Cyclin D1

Share to Cyclin-Dependent Kinase Inhibitor p21

Share to Cyclins

Share to Enzyme Activation

Source

Identifiers

PMID: 15173009
DOI: 10.1158/0008-5472.CAN-03-3740

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Activation of protein kinase G is sufficient to induce apoptosis and inhibit cell migration in colon cancer cells.PMID 15173009Read ↗

Cyclic GMP-dependent protein kinase activation and induction by exisulind and CP461 in colon tumor cells.Semantic proximity Read ↗

Mice expressing activated PI3K rapidly develop advanced colon cancer.Semantic proximity Read ↗

Selective inhibition of proliferation in colorectal carcinoma cell lines expressing mutant APC or activated B-Raf.Semantic proximity Read ↗

Epithelial-to-Mesenchymal Transition and Oncogenic Ras Expression in Resistance to the Protein Kinase Cβ Inhibitor Enzastaurin in Colon Cancer CellsSemantic proximity Read ↗

PI3K/Akt and GSK-3β prevents in a differential fashion the malignant phenotype of colorectal cancer cells.Semantic proximity Read ↗

Oncogenic Ras promotes butyrate-induced apoptosis through inhibition of gelsolin expression.Semantic proximity Read ↗

Blocking phosphoinositide 3-kinase activity in colorectal cancer cells reduces proliferation but does not increase apoptosis alone or in combination with cytotoxic drugs.Semantic proximity Read ↗

Apremilast Induces Apoptosis of Human Colorectal Cancer Cells with Mutant KRAS.Semantic proximity Read ↗

Vasodilator-stimulated phosphoprotein (VASP) phosphorylation provides a biomarker for the action of exisulind and related agents that activate protein kinase G.Semantic proximity Read ↗

Specific inhibition of p110α subunit of PI3K: putative therapeutic strategy for KRAS mutant colorectal cancers.Semantic proximity Read ↗

Colon carcinoma cells harboring PIK3CA mutations display resistance to growth factor deprivation induced apoptosis.Semantic proximity Read ↗

Proof-of-principle: oncogenic beta-catenin is a valid molecular target for the development of pharmacological inhibitors.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.