Related Experiment Video

Updated: Aug 18, 2026

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
06:54

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells

Published on: October 27, 2020

Gamma-tocotrienol inhibits neoplastic mammary epithelial cell proliferation by decreasing Akt and nuclear factor

Sumit J Shah1, Paul W Sylvester

  • 1School of Pharmacy, 700 University Avenue, University of Louisiana at Monroe, Monroe, LA 71209-0470, USA.

Experimental Biology and Medicine (Maywood, N.J.)
|March 29, 2005
PubMed

Insights

Gamma-tocotrienol, a vitamin E compound, inhibits cancer cell growth by reducing Akt and nuclear factor kappaB (NFkappaB) activity. This study elucidates the molecular mechanisms behind its antiproliferative effects in mammary epithelial cells.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cancer Research

Background:

  • Tocotrienols, a vitamin E subgroup, exhibit anticancer properties by inhibiting neoplastic mammary epithelial cell proliferation.
  • The precise intracellular mechanisms underlying tocotrienol's antiproliferative effects remain largely unknown.
  • Akt and NFkappaB signaling pathways are critical regulators of mammary tumor cell proliferation and survival.

Purpose of the Study:

  • To investigate the effects of gamma-tocotrienol on Akt and NFkappaB activity in neoplastic +SA mammary epithelial cells.
  • To elucidate the molecular mechanisms by which gamma-tocotrienol mediates its antiproliferative effects.

Main Methods:

  • MTT colorimetric assay to assess cell growth inhibition.
  • Immunocytochemical staining for proliferating cell nuclear antigen to evaluate mitotic activity.
  • Western blot analysis to measure levels of activated PI3K-dependent kinase 1 (phospho-PDK-1) and Akt, and kinase activity.
  • Assays to determine NFkappaB transcriptional activity and IkappaB-kinase-alpha/beta activation.

Main Results:

  • Gamma-tocotrienol treatment caused a dose-responsive inhibition of +SA cell growth and mitotic activity.
  • A significant reduction in activated PI3K-dependent kinase 1 (phospho-PDK-1) and Akt levels, along with decreased phospho-Akt kinase activity, was observed.
  • Gamma-tocotrienol suppressed NFkappaB transcriptional activity by inhibiting IkappaB-kinase-alpha/beta activation.
  • These effects were independent of PTEN or protein phosphatase type 2A activity.

Conclusions:

  • Gamma-tocotrienol exhibits potent antiproliferative effects on neoplastic mammary epithelial cells.
  • The antiproliferative action of gamma-tocotrienol is mediated, at least in part, by the downregulation of Akt and NFkappaB signaling pathways.
  • These findings provide mechanistic insights into the anticancer potential of tocotrienols.

More Related Videos

Multiomics Analysis of TMEM200A as a Pan-Cancer Biomarker07:47

Multiomics Analysis of TMEM200A as a Pan-Cancer Biomarker

Published on: September 15, 2023

Using Mouse Mammary Tumor Cells to Teach Core Biology Concepts: A Simple Lab Module10:39

Using Mouse Mammary Tumor Cells to Teach Core Biology Concepts: A Simple Lab Module

Published on: June 18, 2015

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...
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...
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...
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...
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...
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...