scispace - formally typeset
P

Pithi Chanvorachote

Researcher at Chulalongkorn University

Publications -  217
Citations -  4635

Pithi Chanvorachote is an academic researcher from Chulalongkorn University. The author has contributed to research in topics: Cancer cell & Cancer. The author has an hindex of 31, co-authored 182 publications receiving 3557 citations. Previous affiliations of Pithi Chanvorachote include West Virginia University.

Papers
More filters
Journal ArticleDOI

Silver nanoparticles induce toxicity in A549 cells via ROS-dependent and ROS-independent pathways

TL;DR: Observations allow us to propose that the in vitro toxic effects of AgNPs on A549 cells are mediated via both ROS-dependent (cytotoxicity) and ROS-independent (cell cycle arrest) pathways.
Journal ArticleDOI

Reactive Oxygen Species Mediate Caspase Activation and Apoptosis Induced by Lipoic Acid in Human Lung Epithelial Cancer Cells through Bcl-2 Down-Regulation

TL;DR: A novel pro-oxidant role of LA is indicated in apoptosis induction and its regulation by Bcl-2, which may be exploited for the treatment of cancer and related apoptosis disorders.
Journal ArticleDOI

Regulation of Lung Cancer Cell Migration and Invasion by Reactive Oxygen Species and Caveolin-1

TL;DR: It is demonstrated here that Cav-1 plays an important role in the migration and invasion of human lung carcinoma H460 cells and that these effects are differentially regulated by cellular ROS.
Journal ArticleDOI

Nitric Oxide Regulates Cell Sensitivity to Cisplatin-Induced Apoptosis through S-Nitrosylation and Inhibition of Bcl-2 Ubiquitination

TL;DR: It is shown that NO impairs the apoptotic function of cells and increases their resistance to cisplatin-induced cell death in human lung carcinoma H-460 cells, indicating a novel pathway for NO regulation of Bcl-2, which provides a key mechanism for cisPlatin resistance and its potential modulation for improved cancer chemotherapy.
Journal ArticleDOI

Nitric oxide negatively regulates Fas CD95-induced apoptosis through inhibition of ubiquitin-proteasome-mediated degradation of FLICE inhibitory protein

TL;DR: It is shown that stimulation of the Fas receptor by its ligand (FasL) results in rapid generation of NO and concomitant decrease in cellular FLICE inhibitory protein (FLIP) expression without significant effect on Fas and Fas-associated death domain (FADD) adapter protein levels, indicating a novel pathway for NO regulation of FLIP.