Related Experiment Video

Updated: May 29, 2026

Induction of Invasive Transitional Cell Bladder Carcinoma in Immune Intact Human MUC1 Transgenic Mice: A Model for Immunotherapy Development
11:02

Induction of Invasive Transitional Cell Bladder Carcinoma in Immune Intact Human MUC1 Transgenic Mice: A Model for Immunotherapy Development

Published on: October 30, 2013

Bufalin induces apoptosis through activation of both the intrinsic and extrinsic pathways in human

Su-Hyun Hong1, Yung Hyun Choi

  • 1Department of Biochemistry, College of Oriental Medicine, Research Institute of Oriental Medicine, Dong-Eui University, Busan 614-052, Republic of Korea.

Oncology Reports
|September 9, 2011
PubMed

Insights

Bufalin, derived from toad venom, effectively inhibits T24 human bladder cancer cell growth. It induces apoptosis and cell cycle arrest at the G2/M phase through both intrinsic and extrinsic pathways.

Area of Science:

  • Pharmacology
  • Oncology
  • Molecular Biology

Background:

  • Bufalin, a component of the Chinese medicine Chansu from toad venom, exhibits potential anticancer activity in vitro.
  • The precise molecular mechanisms underlying bufalin's induction of apoptosis remain largely unelucidated.

Purpose of the Study:

  • To investigate the apoptosis-inducing effects of bufalin on T24 human bladder cancer cells.
  • To elucidate the molecular mechanisms by which bufalin mediates cancer cell death.

Main Methods:

  • T24 human bladder cancer cells were treated with varying concentrations of bufalin.
  • Analysis included cell cycle progression, apoptosis markers (apoptotic bodies, chromatin condensation, sub-G1 accumulation), caspase activation (caspase-3, -8, -9), PARP degradation, mitochondrial membrane potential, Bax/Bcl-2 ratio, IAP family members, and death receptor factors.

Main Results:

  • Bufalin treatment inhibited T24 cell growth in a dose-dependent manner, inducing G2/M cell cycle arrest and apoptosis.
  • Apoptosis was mediated by activation of caspase-3, -8, and -9, PARP cleavage, mitochondrial dysfunction, altered Bax/Bcl-2 ratio, and modulation of IAP family members and death receptors.
  • Bufalin triggers apoptosis via both intrinsic and extrinsic pathways, blocking cell cycle progression.

Conclusions:

  • Bufalin effectively inhibits human bladder cancer cell growth by inducing apoptosis and cell cycle arrest.
  • The study clarifies bufalin's anticancer mechanism, involving both intrinsic and extrinsic apoptotic pathways.
  • Bufalin represents a promising therapeutic agent for bladder cancer, warranting further investigation.

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...
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...
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 reduction of the tissue.
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
Caspases01:24

Caspases

Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside cells.