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The Intrinsic Apoptotic Pathway

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...

Apoptosis

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.

The Extrinsic Apoptotic Pathway

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 Autophagy

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...

Caspases

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.

Phagocytosis of Apoptotic Cells

Phagocytosis of Apoptotic Cells

Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or immature dendritic cells. Non-professional phagocytes such as epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes.
Normal cells contain receptors that prevent them from being recognized by phagocytes.

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Related Experiment Video

Updated: May 23, 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

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

[Prostate cancer and apoptosis].

Adriana Mayora¹, Francisco Arvelo

¹Postgrado de Biología Celular, Facultad de Ciencias, Universidad Central de Venezuela.

Investigacion Clinica

|April 25, 2012

Summary

Prostate cancer growth relies on the androgen receptor (AR). This review explores how prostate cancer cells resist AR-targeted therapies and evade cell death.

Area of Science:

Oncology
Molecular Biology
Endocrinology

Context:

Advanced prostate cancer treatment relies on androgen pathway blockage.
Prostate cancer often becomes resistant to hormone therapy over time.
Understanding resistance mechanisms is crucial for improving patient outcomes.

Purpose:

To review the molecular mechanisms driving prostate cancer progression.
To examine how prostate cancer cells evade apoptosis and develop resistance.
To provide insights into AR-dependent and AR-independent resistance pathways.

Summary:

Prostate cancer growth is androgen receptor (AR)-dependent, making AR pathway blockage a standard treatment.
Resistance develops through AR gene amplification, mutations, increased co-activators, or AR phosphorylation.

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Quantitative Analysis of Autophagy using Advanced 3D Fluorescence Microscopy

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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

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Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

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Quantitative Analysis of Autophagy using Advanced 3D Fluorescence Microscopy

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Published on: May 3, 2013

AR-independent pathways, like neuroendocrine differentiation, also contribute to treatment failure.

Cancer cells employ mechanisms to evade apoptosis, further complicating treatment.

Impact:

This review highlights key molecular targets for overcoming treatment resistance in advanced prostate cancer.
Understanding these mechanisms can guide the development of novel therapeutic strategies.
Insights into AR signaling and resistance pathways are vital for future prostate cancer research.