Related Experiment Video

Updated: Feb 25, 2026

Author Spotlight: Exploring the Role of FAM83A in Cervical Cancer
04:20

Author Spotlight: Exploring the Role of FAM83A in Cervical Cancer

Published on: February 9, 2024

1.5K

Nitric oxide induces oral squamous cell carcinoma cells apoptosis with p53 accumulation

Shi-fang Zhao1, Xiao-yan Tong, Fu-dong Zhu

  • 1Department of Oral and Maxillofacial Surgery, School of Stomatology, Zhejiang University, Hangzhou, China. zju_txy@hotmail.com

Oral Oncology
|June 28, 2005
PubMed

Insights

Exogenous nitric oxide inhibits oral cancer cell proliferation and induces apoptosis, potentially through the p53 pathway. This study explored nitric oxide

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Nitric oxide (NO) exhibits cytotoxic effects on various tumor cells.
  • Understanding NO's role in oral cancer is crucial for therapeutic development.

Purpose of the Study:

  • To investigate the effects of exogenous nitric oxide on oral squamous cell carcinoma (OSCC) apoptosis.
  • To elucidate the underlying mechanisms, including the involvement of p53 and inducible nitric oxide synthase (iNOS).

Main Methods:

  • Tca8113 OSCC cells were treated with nitric oxide released from sodium nitroprusside (SNP).
  • Cell proliferation was assessed using MTT assay.
  • Apoptosis was detected by flow cytometry, and p53 and iNOS expression were analyzed via Western blot and immunocytochemistry, respectively.

Main Results:

  • SNP released nitric oxide in a dose-dependent manner.
  • Exogenous nitric oxide significantly inhibited Tca8113 cell proliferation and induced apoptosis in a dose- and time-dependent manner.
  • p53 expression increased with elevated apoptosis, while iNOS expression remained unchanged.

Conclusions:

  • Exogenous nitric oxide inhibits OSCC cell proliferation and induces apoptosis, likely via a p53-dependent pathway.
  • The study suggests a potential therapeutic role for nitric oxide in OSCC treatment.
  • Nitric oxide's effect on OSCC does not appear to involve significant modulation of iNOS protein levels.

More Related Videos

Yeast As a Chassis for Developing Functional Assays to Study Human P5314:57

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

10.1K
Identification of OTX1 and OTX2 As Two Possible Molecular Markers for Sinonasal Carcinomas and Olfactory Neuroblastomas07:00

Identification of OTX1 and OTX2 As Two Possible Molecular Markers for Sinonasal Carcinomas and Olfactory Neuroblastomas

Published on: February 28, 2019

6.3K

Related Concept Videos

The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
8.8K
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
5.3K
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
9.0K
Nitric Oxide Signaling Pathway01:28

Nitric Oxide Signaling Pathway

Nitric oxide (NO), an inorganic gas, acts as a potent second messenger in most animal and plant tissues. NO diffuses out of the cells that produce it and enters the neighboring cells to generate a downstream response. NO synthase (NOS) catalyzes NO production by the deamination of the amino acid arginine. There are three isoforms of NOS. Endothelial cells have endothelial NOS (eNOS), nerve and muscle cells have neuronal NOS (nNOS), and macrophages produce inducible NOS (iNOS) upon exposure...
6.4K
Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size...
15.7K
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
7.2K