Related Experiment Video

Updated: Jan 17, 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

1.4K

Ketamine Induces Mitochondrial Fission and Dysfunction in Cervical Cancer Cells via RhoA-Dependent DRP-1 Activation

Yanfang Zhou1, Guangming Chen2, Ye Zhu3

  • 1Department of Gynecology, Qianjiang Central Hospital of Hubei Province, Qianjiang, China.

Journal of Biochemical and Molecular Toxicology
|September 21, 2025
PubMed

Insights

Ketamine shows promise for cervical cancer treatment by disrupting mitochondrial function and causing cell death. It targets mitochondrial fragmentation and dysfunction through RhoA signaling, offering a new therapeutic avenue.

Area of Science:

  • Oncology
  • Mitochondrial Biology
  • Pharmacology

Background:

  • Mitochondrial fragmentation and dysfunction are key in cervical cancer progression.
  • Ketamine exhibits anti-cancer properties, including cytotoxicity and apoptosis induction.
  • Ketamine's role in regulating mitochondrial dynamics in cervical cancer is not well understood.

Purpose of the Study:

  • To investigate the effects of ketamine on mitochondrial network dynamics in C33A cervical cancer cells.
  • To elucidate the molecular mechanisms underlying ketamine-induced mitochondrial dysfunction.
  • To explore ketamine's potential as a therapeutic agent for cervical cancer.

Main Methods:

  • Assessed ketamine's cytotoxicity using γ-glutamyl transpeptidase (GGT) and lactate dehydrogenase (LDH) release assays.
  • Evaluated mitochondrial function by measuring Complex IV activity, mitochondrial membrane potential (MMP), and ATP production.
  • Analyzed mitochondrial fragmentation and key protein expressions (p-Drp1, DRP-1, CaMK II, RhoA, Rac1/Cdc42).

Main Results:

  • Ketamine demonstrated dose-dependent cytotoxicity in C33A cells, reducing viability.
  • Ketamine (100 μM) induced mitochondrial dysfunction, characterized by decreased Complex IV activity, MMP, ATP production, and increased fragmentation.
  • Ketamine upregulated p-Drp1, CaMK II, and RhoA; RhoA inhibition attenuated ketamine-induced mitochondrial changes.

Conclusions:

  • Ketamine exerts significant cytotoxic effects on cervical cancer cells by inducing mitochondrial fragmentation and dysfunction.
  • RhoA acts as a crucial mediator in ketamine's effects on mitochondrial dynamics.
  • Ketamine represents a potential therapeutic strategy targeting mitochondrial pathways in cervical cancer.
Keywords:
Cervical CancerDrp1KetamineMitochondrial fragmentationRhoA

More Related Videos

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen19:44

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

19.1K
Detection of Mitochondria Membrane Potential to Study CLIC4 Knockdown-induced HN4 Cell Apoptosis In Vitro13:20

Detection of Mitochondria Membrane Potential to Study CLIC4 Knockdown-induced HN4 Cell Apoptosis In Vitro

Published on: July 17, 2018

10.8K

Related Concept Videos

Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
18.5K
Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists01:28

Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists

Neurokinin 1 (NK1) receptors are distributed across the GI tract, vagal afferents, and key CNS regions including the central vomiting center and chemoreceptor trigger zone (CTZ) Chemotherapy agents stimulate enterochromaffin cells in the gastrointestinal (GI) tract to release large amounts of substance P (SP). SP is a neuropeptide released by specific sensory nerves in response to many different stressors, including those in the GI mucosa affected by chemotherapy.  SP binds and activates...
589
Drugs that Destabilize Microtubules01:10

Drugs that Destabilize Microtubules

Microtubules are dynamic structures and can be regulated by microtubule targeting agents (MTAs). Microtubule destabilizing drugs are a class of MTAs that destabilize and prevent microtubules' polymerization. Both natural and synthetic chemicals can be found under this class of drugs. Vincristine and vinblastine, two vinca alkaloids, and colchicine were among the first to be discovered. These drugs can affect cells in various ways, either by inducing a change in cell morphology, preventing...
3.6K
Destabilization of Microtubules01:45

Destabilization of Microtubules

The destabilization of microtubules can occur during different stages of the microtubule lifecycle, such as nucleation or elongation. It can take place at either end of the microtubule or in the microtubule lattices as a whole. The lifespan of individual microtubules within a cell varies according to the cell type and stage of the cell cycle. During interphase, the lifespan of the microtubule is about 30 minutes, while during cell division, it is about 15 minutes. In axonal microtubules of...
3.5K