Related Experiment Video
Updated: May 11, 2026

Cell Population Analyses During Skin Carcinogenesis
Published on: August 21, 2013
Transgenic human programmed cell death 5 expression in mice suppresses skin cancer development by enhancing apoptosis
Yanhui Li1, Gang Zhou, Lijun La
1Department of Medical Genetics, School of Basic Sciences, Peking University Health Science Center, Beijing, China.
Aims:
We sought to probe the role of human programmed cell death 5 (PDCD5) in vivo and to understand its mechanisms.
Main Methods:
A transgenic mouse model of human PDCD5 was generated by pronuclear microinjection. Apoptosis in tissues of three independent transgenic mouse lines was quantified by terminal deoxynucleotidyl transferase mediated dUTP Nick End Labeling (TUNEL) and compared to wild type littermates. Their lifespan was compared. 8-Week PDCD5 mice and wild type mice (at a group of 5) were treated with carcinogen 3-methylcholanthrene (3-MC) at 5 μg per week to induce skin cancer. Cancer development was measured by examining hematoxylin and eosin (H&E) stained skin sections after 5 weeks and 10 weeks treatment. Protein expression was determined by Western blot and apoptosis of skin cells was quantified by TUNEL.
Key Findings:
Starting from 5 months after birth, significant autonomous apoptosis was observed in multiple tissues of transgenic mice including skin, liver, spleen, adrenal gland and thyroid gland comparing to their wild type littermates. The average lifespan of PDCD5 mice was reduced to 9.75 months (normally 24-30 months). Moreover, carcinogen 3-MC induced skin cancer development was attenuated in the lesion of PDCD5 transgenic mice by enhancing apoptosis. Pro-apoptotic protein Bax expression was up-regulated in the 3-MC treated skin of transgenic mice.
Significance:
These results suggest PDCD5 plays an antitumor role by enhancing apoptosis in animal physiological settings. Therefore, PDCD5 is a potential target for cancer therapy.
Insights
Human programmed cell death 5 (PDCD5) enhances apoptosis in vivo, reducing tumor development. This suggests PDCD5 is a promising target for novel cancer therapies.
Area of Science:
- Molecular Biology
- Cell Biology
- Oncology
Background:
- Programmed cell death 5 (PDCD5) is a protein involved in apoptosis.
- Its precise role in vivo and mechanisms remain to be fully elucidated.
Purpose of the Study:
- To investigate the in vivo function of human programmed cell death 5 (PDCD5).
- To understand the underlying mechanisms of PDCD5's role in apoptosis and cancer development.
Main Methods:
- Generated a transgenic mouse model expressing human PDCD5.
- Quantified apoptosis using TUNEL assay and compared lifespan with wild-type littermates.
- Induced skin cancer with 3-methylcholanthrene (3-MC) and assessed tumor development via histology and protein analysis.
Main Results:
- Transgenic mice exhibited increased spontaneous apoptosis in multiple tissues.
- PDCD5 expression reduced lifespan but attenuated 3-MC-induced skin cancer by enhancing apoptosis.
- Upregulation of pro-apoptotic protein Bax was observed in treated skin.
Conclusions:
- PDCD5 demonstrates an antitumor role in vivo by promoting apoptosis.
- PDCD5 represents a potential therapeutic target for cancer treatment.
Related Concept Videos
Mouse Models of Cancer Study
The development of transgenic, knockout, and knock-in mice has led to an exponential increase in their use as model organisms in research,...
In-vitro Mutagenesis
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...
Abnormal Proliferation
The Extrinsic Apoptotic Pathway
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...

