Related Experiment Video

Updated: Jun 12, 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

Sorafenib induces apoptosis and autophagy in prostate cancer cells in vitro

Anders Ullén1, Marianne Farnebo, Lena Thyrell

  • 1Department of Oncology-Pathology, Cancer Centrum Karolinska, Karolinska Institutet, 17176 Stockholm, Sweden. anders.ullen@karolinska.se

International Journal of Oncology
|June 2, 2010
PubMed

Insights

Sorafenib, a tyrosine kinase inhibitor, reduces prostate cancer cell viability and induces apoptosis. This study reveals sorafenib also triggers autophagy, a novel anticancer mechanism.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Sorafenib, a multi-kinase inhibitor, shows clinical efficacy in advanced prostate cancer.
  • Investigating sorafenib's molecular anti-tumoral effects on prostate cancer cell lines is crucial.

Purpose of the Study:

  • To evaluate the anti-tumoral properties of sorafenib on prostate cancer cell lines.
  • To investigate sorafenib's effects on MAPK pathway, apoptosis, and autophagy.

Main Methods:

  • Utilized hormone-refractory (PC3, DU145) and hormone-responsive (22Rv1) prostate cancer cell lines.
  • Employed immunoblotting, flow cytometry, and immunocytochemistry to assess molecular changes.
  • Evaluated effects on the MAPK pathway, apoptosis, and autophagy.

Main Results:

  • Sorafenib dose-dependently reduced cell viability in prostate cancer cell lines.
  • Sorafenib induced apoptosis and inactivated the MAPK pathway.
  • Sorafenib treatment was shown to induce cellular autophagy for the first time.

Conclusions:

  • Sorafenib exhibits anti-cancer potential through multiple mechanisms, including apoptosis and MAPK inhibition.
  • Sorafenib induces autophagy in prostate cancer cells, representing a novel effector mechanism.
  • Findings suggest potential therapeutic combinations involving autophagy-modulating agents to enhance sorafenib's efficacy.

More Related Videos

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

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...
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 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...
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...
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...