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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...
Drugs that Stabilize Microtubules01:15

Drugs that Stabilize Microtubules

Microtubules are dynamic structures that undergo cycles of catastrophe and rescue. The microtubules play a central role in cell division by forming the spindle apparatus for segregating the chromosomes. This makes them ideal targets for regulating dividing cells in tumors and malignant cancer cells. Microtubule stabilizing drugs help stabilize the microtubule formation and promote its polymerization. Paclitaxel was the first microtubule stabilizing agent used as anticancer drug in chemotherapy...
Combination Therapies and Personalized Medicine02:50

Combination Therapies and Personalized Medicine

Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...
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...

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Related Experiment Video

Updated: Jul 4, 2026

An In Vitro Model for Studying Cellular Transformation by Kaposi Sarcoma Herpesvirus
09:53

An In Vitro Model for Studying Cellular Transformation by Kaposi Sarcoma Herpesvirus

Published on: August 25, 2017

Paclitaxel Induces Apoptosis in AIDS-Related Kaposi's Sarcoma Cells.

J Cai1, T Zheng, R Masood

  • 1Departments of Medicine University of Southern California Kenneth Norris Comprehensive Cancer Center and Research Institute Los Angeles CA USA.

Sarcoma
|June 4, 2008
PubMed
Summary

Paclitaxel effectively treats Kaposi's sarcoma (KS) by inducing apoptosis and inhibiting KS cell migration and tumor growth. This microtubule-stabilizing drug offers a promising therapeutic avenue for KS patients.

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Identifying Dysregulated Genes Induced by Kaposi's Sarcoma-associated Herpesvirus (KSHV)
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Published on: September 14, 2010

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Last Updated: Jul 4, 2026

An In Vitro Model for Studying Cellular Transformation by Kaposi Sarcoma Herpesvirus
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Identifying Dysregulated Genes Induced by Kaposi's Sarcoma-associated Herpesvirus (KSHV)
07:02

Identifying Dysregulated Genes Induced by Kaposi's Sarcoma-associated Herpesvirus (KSHV)

Published on: September 14, 2010

Area of Science:

  • Oncology
  • Pharmacology
  • Cell Biology

Background:

  • Paclitaxel is a microtubule-stabilizing agent with known anti-cancer properties.
  • AIDS-related Kaposi's sarcoma (KS) is characterized by endothelial cell proliferation and shares markers with activated endothelial cells.
  • Paclitaxel demonstrates antiangiogenic activity by disrupting cytoskeletal structure, impacting cell migration and invasion.

Purpose of the Study:

  • To elucidate the mechanism of paclitaxel's anti-tumor effects in Kaposi's sarcoma.
  • To evaluate the efficacy of paclitaxel in inhibiting KS cell growth and migration in vitro and in vivo.

Main Methods:

  • In vitro studies assessed KS cell sensitivity to paclitaxel, growth inhibition, migration inhibition, and apoptosis markers (Bcl-2, Bcl-xL, cytochrome c, caspase-3).
  • In vivo studies utilized nude mouse xenograft models to evaluate paclitaxel's effect on tumor growth.
  • Histological analysis examined tumor proliferative index, mitotic figures, and apoptotic cell counts.

Main Results:

  • Paclitaxel exhibited high sensitivity in KS cells (half-maximal growth inhibition at 0.8 nM) and inhibited cell migration.
  • Paclitaxel induced cell cycle arrest (sub-G1) and apoptosis in vitro, evidenced by Bcl-2/Bcl-xL phosphorylation, cytochrome c release, and caspase-3 activation.
  • In vivo, paclitaxel (10 mg/kg) reduced tumor growth by 75% and decreased proliferation while increasing apoptosis in KS xenografts.

Conclusions:

  • Paclitaxel effectively inhibits Kaposi's sarcoma cell proliferation, migration, and tumor growth through apoptosis induction.
  • The findings support paclitaxel as a potent therapeutic agent for AIDS-related Kaposi's sarcoma.
  • Paclitaxel's mechanism involves microtubule stabilization, cell cycle arrest, and induction of apoptotic pathways.