Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Overview of Cell Death01:30

Overview of Cell Death

Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the 20th century...
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 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...
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...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Editorial expression of concern: Resveratrol enhances prostate cancer cell response to ionizing radiation. Modulation of the AMPK, Akt and mTOR pathways.

Radiation oncology (London, England)·2026
Same author

Anticancer properties of ethanolic extract of Omani <i>Ocimum basilicum</i> in HCT116 colorectal cancer cells.

Open veterinary journal·2026
Same author

Association between paraspinal muscle quality and surgery for adjacent segment disease.

North American Spine Society journal·2025
Same author

Development of a direct competitive enzyme-linked immunosorbent assay (dc-ELISA) for the detection of scopolamine in wheat.

Food additives & contaminants. Part A, Chemistry, analysis, control, exposure & risk assessment·2024
Same author

Risk Factors for Sacroiliac Joint Fusion after Instrumented Spinal Fusion.

Global spine journal·2024
Same author

Computational modeling to study the impact of changes in Nav1.8 sodium channel on neuropathic pain.

Frontiers in computational neuroscience·2024

Related Experiment Video

Updated: Jun 12, 2026

Cell Death Associated with Abnormal Mitosis Observed by Confocal Imaging in Live Cancer Cells
15:53

Cell Death Associated with Abnormal Mitosis Observed by Confocal Imaging in Live Cancer Cells

Published on: August 21, 2013

Metronomic PDT and cell death pathways.

Gurmit Singh1, Omar Alqawi, Myrna Espiritu

  • 1Department of Pathology and Molecular Medicine, Juravinski Cancer Centre, McMaster University, Hamilton, ON, Canada.

Methods in Molecular Biology (Clifton, N.J.)
|June 17, 2010
PubMed
Summary

Metronomic Aminolevulinic Acid-Photodynamic Therapy (ALA-PDT) induces apoptosis in glioma cells by inhibiting LTbetaR and NF-kappaB. This low-dose, continuous treatment offers a promising strategy for brain tumor therapy.

More Related Videos

LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation
06:12

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

Published on: May 3, 2024

One-step Protocol for Evaluation of the Mode of Radiation-induced Clonogenic Cell Death by Fluorescence Microscopy
06:47

One-step Protocol for Evaluation of the Mode of Radiation-induced Clonogenic Cell Death by Fluorescence Microscopy

Published on: October 23, 2017

Related Experiment Videos

Last Updated: Jun 12, 2026

Cell Death Associated with Abnormal Mitosis Observed by Confocal Imaging in Live Cancer Cells
15:53

Cell Death Associated with Abnormal Mitosis Observed by Confocal Imaging in Live Cancer Cells

Published on: August 21, 2013

LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation
06:12

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

Published on: May 3, 2024

One-step Protocol for Evaluation of the Mode of Radiation-induced Clonogenic Cell Death by Fluorescence Microscopy
06:47

One-step Protocol for Evaluation of the Mode of Radiation-induced Clonogenic Cell Death by Fluorescence Microscopy

Published on: October 23, 2017

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Metronomic chemotherapy, a continuous low-dose administration, minimizes side effects.
  • Metronomic dosing in Photodynamic Therapy (PDT) aims to enhance tumor-specific apoptosis.
  • ALA-PDT utilizes aminolevulinic acid and light to induce cell death.

Purpose of the Study:

  • To investigate the molecular mechanisms of apoptosis induced by metronomic ALA-PDT in glioma cells.
  • To compare acute PDT with metronomic PDT in U87 (human) and CNS-1 (rat) glioma cell lines.
  • To identify specific cell death pathways activated by metronomic ALA-PDT.

Main Methods:

  • Treatment of U87 and CNS-1 glioma cells with acute and metronomic ALA-PDT.
  • Microarray analysis of gene expression in glioblastoma cells treated with metronomic ALA-PDT.
  • Assessment of apoptosis pathways, including LTbetaR and NF-kappaB signaling.

Main Results:

  • Metronomic ALA-PDT induced apoptosis in both human (U87) and rat (CNS-1) glioma cell lines.
  • Gene expression analysis revealed that metronomic ALA-PDT inhibits the LTbetaR pathway.
  • The apoptosis mechanism was linked to the inhibition of the transcription factor NF-kappaB in an ALA concentration-dependent manner.

Conclusions:

  • Metronomic ALA-PDT effectively triggers apoptosis in glioma cells through LTbetaR and NF-kappaB inhibition.
  • This low-dose, continuous PDT approach shows potential for targeted brain tumor treatment.
  • The findings elucidate the molecular underpinnings of metronomic ALA-PDT, supporting its therapeutic application.