Long-term nitric oxide exposure enhances lung cancer cell migration

Arpasinee Sanuphan, Preedakorn Chunhacha, Varisa Pongrakhananon, Pithi Chanvorachote

Research output: Contribution to journalArticle

26 Citations (Scopus)

Abstract

Nitric oxide (NO) found in the vicinity of lung cancer cells may play a role in the regulation of cancer cell behaviors. To explore the possible effects of NO on cell motility, human lung cancer cells were exposed to nontoxic concentrations of NO for 0-14 days, and the migratory characteristics of the cells were determined. The present study found that long-term treatment with NO significantly enhanced cell migration in a dose- and time-dependent manner. Furthermore, we found that the increased migratory action was associated with the increased expression of caveolin-1 (Cav-1), which in turn activated the focal adhesion kinase (FAK) and ATP-dependent tyrosine kinase (Akt) pathways. Notably, the NO-treated cells exhibited an increased number of filopodia per cell, as well as an increase in the levels of cell division cycle 42 (Cdc42) protein. Together, these results indicate that extended NO exposure has a novel effect on cell migration through a Cav-1-dependent mechanism, a finding that strengthens our understanding of cancer biology.

Original languageEnglish (US)
Article number186972
JournalBioMed Research International
Volume2013
DOIs
StatePublished - 2013
Externally publishedYes

Fingerprint

Cell Movement
Lung Neoplasms
Nitric Oxide
Cells
Caveolin 1
Focal Adhesion Protein-Tyrosine Kinases
Cell Cycle Proteins
Pseudopodia
Protein-Tyrosine Kinases
Neoplasms
Adenosine Triphosphate

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Immunology and Microbiology(all)
  • Medicine(all)

Cite this

Sanuphan, A., Chunhacha, P., Pongrakhananon, V., & Chanvorachote, P. (2013). Long-term nitric oxide exposure enhances lung cancer cell migration. BioMed Research International, 2013, [186972]. https://doi.org/10.1155/2013/186972

Long-term nitric oxide exposure enhances lung cancer cell migration. / Sanuphan, Arpasinee; Chunhacha, Preedakorn; Pongrakhananon, Varisa; Chanvorachote, Pithi.

In: BioMed Research International, Vol. 2013, 186972, 2013.

Research output: Contribution to journalArticle

Sanuphan, A, Chunhacha, P, Pongrakhananon, V & Chanvorachote, P 2013, 'Long-term nitric oxide exposure enhances lung cancer cell migration', BioMed Research International, vol. 2013, 186972. https://doi.org/10.1155/2013/186972
Sanuphan, Arpasinee ; Chunhacha, Preedakorn ; Pongrakhananon, Varisa ; Chanvorachote, Pithi. / Long-term nitric oxide exposure enhances lung cancer cell migration. In: BioMed Research International. 2013 ; Vol. 2013.
@article{b82243098449464393465b1339fbc7fa,
title = "Long-term nitric oxide exposure enhances lung cancer cell migration",
abstract = "Nitric oxide (NO) found in the vicinity of lung cancer cells may play a role in the regulation of cancer cell behaviors. To explore the possible effects of NO on cell motility, human lung cancer cells were exposed to nontoxic concentrations of NO for 0-14 days, and the migratory characteristics of the cells were determined. The present study found that long-term treatment with NO significantly enhanced cell migration in a dose- and time-dependent manner. Furthermore, we found that the increased migratory action was associated with the increased expression of caveolin-1 (Cav-1), which in turn activated the focal adhesion kinase (FAK) and ATP-dependent tyrosine kinase (Akt) pathways. Notably, the NO-treated cells exhibited an increased number of filopodia per cell, as well as an increase in the levels of cell division cycle 42 (Cdc42) protein. Together, these results indicate that extended NO exposure has a novel effect on cell migration through a Cav-1-dependent mechanism, a finding that strengthens our understanding of cancer biology.",
author = "Arpasinee Sanuphan and Preedakorn Chunhacha and Varisa Pongrakhananon and Pithi Chanvorachote",
year = "2013",
doi = "10.1155/2013/186972",
language = "English (US)",
volume = "2013",
journal = "BioMed Research International",
issn = "2314-6133",
publisher = "Hindawi Publishing Corporation",

}

TY - JOUR

T1 - Long-term nitric oxide exposure enhances lung cancer cell migration

AU - Sanuphan, Arpasinee

AU - Chunhacha, Preedakorn

AU - Pongrakhananon, Varisa

AU - Chanvorachote, Pithi

PY - 2013

Y1 - 2013

N2 - Nitric oxide (NO) found in the vicinity of lung cancer cells may play a role in the regulation of cancer cell behaviors. To explore the possible effects of NO on cell motility, human lung cancer cells were exposed to nontoxic concentrations of NO for 0-14 days, and the migratory characteristics of the cells were determined. The present study found that long-term treatment with NO significantly enhanced cell migration in a dose- and time-dependent manner. Furthermore, we found that the increased migratory action was associated with the increased expression of caveolin-1 (Cav-1), which in turn activated the focal adhesion kinase (FAK) and ATP-dependent tyrosine kinase (Akt) pathways. Notably, the NO-treated cells exhibited an increased number of filopodia per cell, as well as an increase in the levels of cell division cycle 42 (Cdc42) protein. Together, these results indicate that extended NO exposure has a novel effect on cell migration through a Cav-1-dependent mechanism, a finding that strengthens our understanding of cancer biology.

AB - Nitric oxide (NO) found in the vicinity of lung cancer cells may play a role in the regulation of cancer cell behaviors. To explore the possible effects of NO on cell motility, human lung cancer cells were exposed to nontoxic concentrations of NO for 0-14 days, and the migratory characteristics of the cells were determined. The present study found that long-term treatment with NO significantly enhanced cell migration in a dose- and time-dependent manner. Furthermore, we found that the increased migratory action was associated with the increased expression of caveolin-1 (Cav-1), which in turn activated the focal adhesion kinase (FAK) and ATP-dependent tyrosine kinase (Akt) pathways. Notably, the NO-treated cells exhibited an increased number of filopodia per cell, as well as an increase in the levels of cell division cycle 42 (Cdc42) protein. Together, these results indicate that extended NO exposure has a novel effect on cell migration through a Cav-1-dependent mechanism, a finding that strengthens our understanding of cancer biology.

UR - http://www.scopus.com/inward/record.url?scp=84883193137&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84883193137&partnerID=8YFLogxK

U2 - 10.1155/2013/186972

DO - 10.1155/2013/186972

M3 - Article

VL - 2013

JO - BioMed Research International

JF - BioMed Research International

SN - 2314-6133

M1 - 186972

ER -