Related Experiment Video

Updated: Jul 9, 2026

A Method for Screening and Validation of Resistant Mutations Against Kinase Inhibitors
12:40

A Method for Screening and Validation of Resistant Mutations Against Kinase Inhibitors

Published on: December 7, 2014

Imatinib interferes with survival of multi drug resistant Kaposi's sarcoma cells

Sabrina Basciani1, Rosa Vona, Paola Matarrese

  • 1Cardiovascular Research Unit, Department of Medical Science, IRCCS San Raffaele, Rome, Italy.

FEBS Letters
|December 7, 2007
PubMed

Insights

Imatinib inhibits platelet-derived growth factor (PDGF) phosphorylation in both normal and multi-drug resistant (MDR) Kaposi sarcoma (KS) cells. This suggests imatinib may help overcome MDR in KS by increasing apoptosis or autophagy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Multi-drug resistance (MDR) is a significant challenge in cancer therapy, where tumor cells evade unrelated drugs.
  • Imatinib, a tyrosine kinase inhibitor, is effective against certain tumors by targeting kinases like Bcr-Abl, c-kit, and PDGF receptors.

Purpose of the Study:

  • To investigate the effect of imatinib on platelet-derived growth factor (PDGF) phosphorylation in both wild-type (wt) and multi-drug resistant (MDR) Kaposi sarcoma (KS) cells.
  • To explore the downstream effects of imatinib, specifically apoptosis and autophagy, in different KS cell types.

Main Methods:

  • Treatment of wt and MDR Kaposi sarcoma (KS) cells with imatinib.
  • Assessment of PDGF phosphorylation levels.
  • Evaluation of apoptosis and autophagy induction.

Main Results:

  • Imatinib effectively inhibited PDGF phosphorylation in both wt and MDR KS cells.
  • In wt KS cells, imatinib treatment led to increased apoptosis.
  • In MDR KS cells, imatinib treatment resulted in increased autophagy.

Conclusions:

  • Imatinib demonstrates efficacy in inhibiting PDGF phosphorylation across different Kaposi sarcoma (KS) cell contexts.
  • The distinct cellular responses (apoptosis vs. autophagy) suggest differential mechanisms for imatinib's action in wt versus MDR KS cells.
  • These findings offer new perspectives on utilizing imatinib to overcome multi-drug resistance (MDR) in Kaposi sarcoma (KS) treatment.

More Related Videos

An In Vitro Model for Studying Cellular Transformation by Kaposi Sarcoma Herpesvirus09:53

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

Published on: August 25, 2017

Related Concept Videos

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...
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...
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
Treatment Resistant Cancers02:56

Treatment Resistant Cancers

Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...