Related Experiment Video

Updated: Apr 27, 2026

Development and Maintenance of a Preclinical Patient Derived Tumor Xenograft Model for the Investigation of Novel Anti-Cancer Therapies
09:29

Development and Maintenance of a Preclinical Patient Derived Tumor Xenograft Model for the Investigation of Novel Anti-Cancer Therapies

Published on: September 30, 2016

13.4K

DADS suppresses human esophageal xenograft tumors through RAF/MEK/ERK and mitochondria-dependent pathways

Xiaoran Yin1, Jun Zhang2, Xiaoning Li3

  • 1Department of Oncology, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710004, China. yinxiaoran@163.com.

International Journal of Molecular Sciences
|July 16, 2014
PubMed

Insights

Diallyl disulfide (DADS), a garlic compound, effectively inhibits esophageal cancer growth and promotes apoptosis in cells and animal models. DADS shows promise as a safe and potent anticancer agent for esophageal carcinoma.

Area of Science:

  • Oncology
  • Pharmacology
  • Biochemistry

Background:

  • Diallyl disulfide (DADS) is a natural organosulfur compound found in garlic with known anticancer properties.
  • The specific anticancer mechanisms of DADS in human esophageal carcinoma, particularly in vivo, remain largely unelucidated.
  • Esophageal carcinoma is a significant global health concern requiring novel therapeutic strategies.

Purpose of the Study:

  • To investigate the anticancer mechanisms of DADS in human esophageal carcinoma cells (ECA109) and in vivo xenograft models.
  • To evaluate the efficacy and safety of DADS as a potential therapeutic agent for esophageal carcinoma.
  • To elucidate the molecular pathways involved in DADS-induced apoptosis and proliferation inhibition.

Main Methods:

  • MTT assays were used to assess cell viability in ECA109 cells and normal liver cells.
  • Annexin V-FITC/propidium iodide (PI) staining and flow cytometry were employed to detect apoptosis.
  • Xenograft studies in nude mice were conducted to evaluate tumor growth inhibition and safety profiles.

Main Results:

  • DADS significantly reduced ECA109 cell viability with minimal toxicity to normal liver cells.
  • DADS induced apoptosis in a dose-dependent manner, confirmed by flow cytometry and caspase-3 inhibition.
  • In vivo, DADS treatment inhibited ECA109 tumor growth, reduced proliferation (PCNA), and activated apoptosis via the mitochondria-dependent pathway, involving caspase-3, p53, Bax/Bcl-2 ratio, and the RAF/MEK/ERK pathway.

Conclusions:

  • DADS demonstrates significant anticancer effects against human esophageal carcinoma in both in vitro and in vivo models.
  • DADS induces apoptosis and inhibits proliferation through specific molecular pathways, including the mitochondria-dependent pathway and modulation of key proteins and signaling cascades.
  • DADS presents as a safe and effective potential therapeutic agent for esophageal carcinoma, warranting further clinical investigation.

More Related Videos

Subculture and Cryopreservation of Esophageal Adenocarcinoma Organoids: Pros and Cons for Single Cell Digestion10:42

Subculture and Cryopreservation of Esophageal Adenocarcinoma Organoids: Pros and Cons for Single Cell Digestion

Published on: July 6, 2022

3.4K
Modeling Oral-Esophageal Squamous Cell Carcinoma in 3D Organoids10:43

Modeling Oral-Esophageal Squamous Cell Carcinoma in 3D Organoids

Published on: December 23, 2022

3.8K

Related Concept Videos

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...
6.3K
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
7.3K