Related Experiment Video

Updated: May 19, 2026

Quantitative Analysis of Autophagy using Advanced 3D Fluorescence Microscopy
09:59

Quantitative Analysis of Autophagy using Advanced 3D Fluorescence Microscopy

Published on: May 3, 2013

Pseudolaric acid B induces caspase-dependent apoptosis and autophagic cell death in prostate cancer cells

Jing Tong1, Shutao Yin, Yinhui Dong

  • 1Division of Nutrition and Health, College of Food Science and Nutritional Engineering, China Agricultural University, Haidian District, Beijing, China.

Phytotherapy Research : PTR
|August 21, 2012
PubMed

Insights

Pseudolaric acid B (PAB) shows significant anti-prostate cancer effects by inducing cell death and halting cell cycle progression. This natural compound also enhances the efficacy of existing cancer therapies.

Area of Science:

  • Natural Products Chemistry
  • Cancer Biology
  • Pharmacology

Background:

  • Pseudolaric acid B (PAB), a terpenoid from medicinal plants, shows potential as a cancer chemopreventive and therapeutic agent.
  • Limited data exists on PAB's efficacy against prostate cancer, necessitating further investigation.

Purpose of the Study:

  • To investigate the anti-prostate cancer effects of Pseudolaric acid B (PAB).
  • To elucidate the mechanisms underlying PAB's action on prostate cancer cells.
  • To evaluate PAB's potential in combination therapy for prostate cancer.

Main Methods:

  • In vitro studies using androgen-dependent (LNCaP) and androgen-independent (PC-3, DU145) prostate cancer cell lines.
  • Analysis of cell cycle progression, apoptosis (caspase-dependent), and autophagic cell death.
  • Assessment of PAB's sensitizing effect on ABT-737-induced cytotoxicity.

Main Results:

  • PAB demonstrated high efficacy against both androgen-dependent and androgen-independent prostate cancer cells.
  • Mechanisms of action included G2/M cell cycle arrest, caspase-dependent apoptosis, and autophagic cell death.
  • PAB significantly enhanced the cytotoxicity of ABT-737 in aggressive prostate cancer cells.

Conclusions:

  • PAB exhibits potent anti-prostate cancer activity through multiple cell death pathways.
  • PAB shows promise as a novel chemopreventive agent for prostate cancer.
  • PAB can act as a therapeutic enhancer, improving the effectiveness of existing drugs against prostate cancer.

More Related Videos

LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation06:12

LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation

Published on: May 3, 2024

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

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...
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.
Autophagic Cell Death01:18

Autophagic Cell Death

Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and pro-apoptotic...
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...
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...
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.