Related Experiment Video

Updated: Jun 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
19:44

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

Thiazole antibiotics target FoxM1 and induce apoptosis in human cancer cells

Uppoor G Bhat1, Marianna Halasi, Andrei L Gartel

  • 1Department of Medicine, University of Illinois at Chicago, Chicago, Illinois, United States of America.

Plos One
|May 15, 2009
PubMed

Insights

Thiazole antibiotics, Siomycin A and thiostrepton, inhibit the oncogenic transcription factor Forkhead box M1 (FoxM1). These compounds induce apoptosis in cancer cells by suppressing FoxM1 expression, suggesting potential as novel anticancer drugs.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Forkhead box M1 (FoxM1) is a transcription factor overexpressed in many human cancers, making it a promising therapeutic target.
  • Previous research identified Siomycin A as an inhibitor of FoxM1 transcriptional activity.

Purpose of the Study:

  • To investigate the effect of thiostrepton, a structural analog of Siomycin A, on FoxM1 activity.
  • To explore the potential of thiazole antibiotics as FoxM1 inhibitors and anticancer agents.

Main Methods:

  • Cell-based assays were used to assess the impact of thiazole antibiotics on FoxM1 transcriptional activity.
  • Western blotting was employed to analyze FoxM1 expression levels.
  • Cancer cell growth inhibition and apoptosis induction assays were performed.

Main Results:

  • Thiostrepton, like Siomycin A, inhibits FoxM1 transcriptional activity.
  • Thiazole antibiotics specifically target FoxM1, not other Forkhead family members or unrelated transcription factors.
  • These antibiotics inhibit FoxM1 expression and induce apoptosis in various human cancer cell lines.
  • Suppression of FoxM1 expression correlates with thiopeptide-induced apoptosis, and FoxM1 overexpression confers partial resistance.

Conclusions:

  • Siomycin A and thiostrepton specifically target FoxM1 to induce cancer cell apoptosis.
  • FoxM1 inhibitors, including thiazole antibiotics, show potential for development as novel anticancer therapeutics.

More Related Videos

Utilizing Functional Genomics Screening to Identify Potentially Novel Drug Targets in Cancer Cell Spheroid Cultures07:48

Utilizing Functional Genomics Screening to Identify Potentially Novel Drug Targets in Cancer Cell Spheroid Cultures

Published on: December 26, 2016

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...
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 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...
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...
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...