Related Experiment Video

Updated: Jun 13, 2026

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen
19:44

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen

Published on: May 30, 2012

Alpha-Tomatine Inhibits Human Oral Epidermoid Carcinoma Cells Through DNA Damage and Activation of Apoptotic

Nihal Ahamed Abulkalam Azad1, Suresh Kathiresan1, Theerthu Azhamuthu1

  • 1Department of Biochemistry and Biotechnology, Faculty of Science, Annamalai University, Tamil Nadu, India.

Journal of Biochemical and Molecular Toxicology
|June 12, 2026
PubMed

Insights

Alpha-tomatine (AT) shows promise as an oral cancer treatment. This natural compound induces cancer cell death through oxidative stress and DNA damage, activating key apoptosis pathways.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Oncology

Background:

  • Oral cancer remains a significant global health challenge with limited treatment options.
  • Alpha-tomatine (AT), a natural glycoalkaloid, exhibits potential anticancer properties.
  • Investigating novel therapeutic agents for oral carcinoma is crucial.

Purpose of the Study:

  • To evaluate the cytotoxic and apoptotic effects of Alpha-tomatine (AT) on KB human oral carcinoma cells.
  • To elucidate the molecular mechanisms underlying AT-induced apoptosis, focusing on oxidative stress and DNA damage.
  • To explore AT's potential as an anticancer agent for oral cancer.

Main Methods:

  • Cytotoxicity was assessed using the MTT assay, determining the IC50 value.
  • Reactive Oxygen Species (ROS) generation was measured via DCFH-DA staining.
  • Apoptosis was evaluated through AO/EtBr and DAPI staining, comet assay for DNA damage, and Western blot analysis for protein expression.

Main Results:

  • AT demonstrated significant cytotoxicity against KB cells with an IC50 of 11.8 µM.
  • AT treatment led to a concentration-dependent increase in ROS levels and induced morphological changes indicative of apoptosis.
  • Western blot analysis revealed downregulation of Bcl-2 and upregulation of p53, Bax, caspase-3, and caspase-9.

Conclusions:

  • Alpha-tomatine effectively triggers apoptosis in oral cancer cells via ROS production and p53 activation.
  • AT-induced apoptosis involves mitochondrial-mediated pathways, leading to DNA fragmentation and caspase activation.
  • AT presents a promising therapeutic candidate for oral cancer treatment.
Keywords:
ROS productionalpha‐tomatineanticancer activityapoptosisoral cancer

More Related Videos

Formation of Covalent DNA Adducts by Enzymatically Activated Carcinogens and Drugs In Vitro and Their Determination by 32P-postlabeling09:33

Formation of Covalent DNA Adducts by Enzymatically Activated Carcinogens and Drugs In Vitro and Their Determination by 32P-postlabeling

Published on: March 20, 2018

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...
Mutagenicity and Carcinogenicity01:25

Mutagenicity and Carcinogenicity

Mutagenicity and carcinogenicity refer to the ability of drugs to cause genetic defects and induce cancer, respectively. The International Agency for Research on Cancer (IARC) classifies agents into four groups based on their carcinogenic potential. Group 1 agents are known human carcinogens; group 2A agents are probably carcinogenic to humans; group 3 agents lack data to support their role in carcinogenesis; and group 4 includes agents for which data support that they are not likely to be...
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
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 daughter...
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...