Related Experiment Video
Updated: Sep 13, 2026

Intramucosal Inoculation of Squamous Cell Carcinoma Cells in Mice for Tumor Immune Profiling and Treatment Response Assessment
Published on: April 22, 2019
Overexpression of tuberous sclerosis complex 2 exerts antitumor effect on oral cancer cell lines
Shin-ichi Kawaguchi1, Koji Harada, Supriatno
1Department of Oral and Maxillofacial Radiology, University of Tokushima, School of Dentistry, 3-18-15 Kuramoto-cho, Tokushima 770-8504, Japan.
Abstract:
Tuberous sclerosis is caused by mutations in tuberous sclerosis complex (TSC) 2 on chromosome 16p13.3, encoding tuberin which is thought to be essential for p27(Kip1) to regulate the cell cycle. In this study, we conducted to examine whether overexpression of TSC2 can affect the growth of oral cancer cells which have different expression level of p27(Kip1) protein. We constructed an expression vector containing sense-oriented rat TSC2 cDNA with pcDNA3.1. We transfected oral cancer cells, B88t (high expression of p27(Kip1) protein) and HI (low expression of p27(Kip1) protein) with the sense expression vector to up-regulate the expression of TSC2 gene. Overexpression of TSC2 exerted the growth inhibitory effect of B88t and HI in vitro and in vivo. These findings suggest that overexpression of TSC2 may exert the antitumor effect on oral cancer cells whether they have high expression of p27(Kip1) protein or not.
Insights
Overexpressing the tuberous sclerosis complex 2 (TSC2) gene inhibits oral cancer cell growth. This antitumor effect occurs regardless of p27(Kip1) protein levels, suggesting TSC2
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Tuberous sclerosis complex 2 (TSC2) gene mutations are linked to tuberous sclerosis.
- TSC2 encodes tuberin, crucial for p27(Kip1)-mediated cell cycle regulation.
- Oral cancer progression may involve dysregulated cell cycle control.
Purpose of the Study:
- To investigate the effect of TSC2 gene overexpression on oral cancer cell growth.
- To determine if p27(Kip1) protein levels influence TSC2's impact on oral cancer cells.
Main Methods:
- Constructed a pcDNA3.1 expression vector with sense-oriented rat TSC2 cDNA.
- Transfected oral cancer cell lines (B88t with high p27(Kip1), HI with low p27(Kip1)) to overexpress TSC2.
- Evaluated the in vitro and in vivo growth inhibitory effects of TSC2 overexpression.
Main Results:
- Overexpression of TSC2 significantly inhibited the growth of both B88t and HI oral cancer cells.
- The growth inhibitory effect of TSC2 was observed in both in vitro and in vivo models.
- TSC2 overexpression demonstrated an antitumor effect irrespective of the initial p27(Kip1) protein expression levels.
Conclusions:
- Overexpression of TSC2 exerts a potent antitumor effect on oral cancer cells.
- The therapeutic potential of TSC2 in oral cancer is independent of p27(Kip1) expression levels.
- Targeting TSC2 warrants further investigation for oral cancer treatment strategies.
Related Concept Videos
Abnormal Proliferation
Cancer-Critical Genes II: Tumor Suppressor Genes
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Cancer-Critical Genes II: Tumor Suppressor Genes
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
Loss of Tumor Suppressor Gene Functions
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
Replicative Cell Senescence

