Pten CKO Mouse Model

The PTEN gene is the first discovered tumor suppressor gene with dual-specific phosphatase activity, and is involved in the regulation of multiple signaling pathways, such as PTEN/PI3K/AKT, PTEN/FAK/P130cas, PTEN/ERK, p53/MDM2, and FRAP/mTOR pathways. The PTEN gene also plays an important role in coordinating cell cycle progression, inhibiting the proliferation and metastasis of cancer cells, and controlling cell adhesion and apoptosis. The mutation, deletion or down-regulation of PTEN gene inactivate the negative regulation on cell growth, thus resulting in the excessive growth of tumor cells that are commonly seen in a variety of primary malignant tumors, such as breast cancer, renal cancer, glioblastoma, endometrial carcinoma and prostate cancer. Known as "a new guardian of the genome", PTEN is one of the two key tumor suppressor genes in the body, with the other being p53.

The homozygous deletion of Pten results in embryonic mortality in mouse, suggesting that PTEN is essential for embryonic development. Mice harboring heterozygous deletion of Pten develop tumors in a number of tissues associated with human.

Our own-developed mouse model of Pten conditional knockout (Pten-CKO) can be mated with mice carrying tissue-specific Cre expression to obtain mice with homozygous deletion of Pten in specific tissues or cells, thus avoiding the embryonic death caused by systemic and homozygous Pten knockout. Pten-CKO mice can be used to study tumorigenesis, anti-tumor targets, neurogenesis, glial differentiation and cerebellar development.

Fig1. The proposed integrative model of tumor suppressor signaling including PTEN and p53. Examples of molecules known to act on DNA damage response, cell proliferation, and cell cycle via the regulatory pathways are shown. Note that some critical pathways have been omitted for clarity.（Int J Oncol. 2014 Jun;44(6):1813-9.）