The Tumor Suppressor Gene PTEN You Must Know

Introduction to PTEN

PTEN gene (chromosome 10 homology loss phosphatase tensin gene), located on human chromosome 10q23.3, contains 9 exons and 8 introns, full-length 200kb, mRNA full-length 5.5kb, molecular weight The 47KD, open reading frame cDNA sequence consisting of 1209 nucleotides encodes a protein with 403 amino acids. The amino-terminal phosphatase domain, the lipid-binding C2 domain, and the carboxyl-terminal domain consisting of about 50 amino acids together constitute the PTEN protein structure related to anti-tumor effects. /Threonine, aminoterminal phosphatase domain for tyrosine dual-specificity phosphatase activity. PTEN is the first tumor suppressor gene with phosphatase activity discovered so far, and it is another tumor suppressor gene closely related to tumorigenesis after p53 gene. PTEN plays a role in cell cycle regulation and rapid cell growth inhibition. play an important role. A large number of studies have found that PTEN gene mutation or deletion exists in various types of cancer, and the abnormal expression of PTEN protein is closely related to the growth, apoptosis, adhesion, migration, infiltration and other processes of cancer cells.

PTEN and cancer

PTEN is under-expressed in various malignant tumors, and its expression products play an important role in the PI3K/Akt signaling pathway. Patients with high PTEN expression in gefitinib-treated NSCLC have better prognosis, and low PTEN expression is associated with gefitinib-acquired resistance. In patients with EGFR mutations, if PTEN is missing, the effect of EGFR-TKI treatment is not good. It may be due to the activation of downstream AKt by PTEN gene, which may lead to cell cycle arrest in G1 phase and induce apoptosis. Akt inhibitors or mTOR inhibitors are potential treatments for PTEN deficiency. PTEN plays a role in genome stability and cell cycle progression. PTEN-deficient cells are more sensitive to DNA damage. PARP inhibitors may be a potential treatment for PTEN-deficient tumors. Everolimus is an inhibitor of mTOR (a serine/threonine kinase downstream of the PI3K/Akt signaling pathway). The CFDA has approved the marketing of everolimus, and the FDA has approved the mTOR inhibitor temsirolimus.

Figure 1. PTEN inhibits the PI3K pathway and downstream oncogenic signaling of AKT. By phosphorylating PIP3, PTEN prevents PDK1 from activating AKT, thereby preventing tumorigenesis.

What's New in PTEN

The phosphoinositide 3-kinase (PI3K)/phosphatase and tensin homolog (PTEN)/Akt axis is a key signaling node regulating key cellular functions, including insulin and other growth factor signaling, lipid and glucose metabolism, as well as cell survival and apoptosis. In this pathway, PTEN acts as a phosphoinositide phosphatase, terminating PI3K-propagated signaling by dephosphorylating PtdIns(3,4)P2 and PtdIns(3,4,5)P3. However, the role of PTEN does not appear to be limited to PI3K signaling antagonism, and new functions for this protein have recently been discovered. In addition to the well-established role of PTEN as a tumor suppressor, there is now increasing evidence that deregulated PTEN expression and/or activity is also implicated in the development of several liver diseases. Dysregulated PTEN expression/activity has been observed in obesity, insulin resistance, diabetes, HBV/HCV infection, and alcoholism, while mutations/deletions have also been associated with hepatocellular carcinoma. Thus, alterations in PTEN expression and activity in hepatocytes appear to be a common and recurring molecular event associated with liver diseases of various etiologies. These recent findings suggest that PTEN may represent a potential co-therapeutic target for many liver diseases.

We can provide diagnostic standards for PTEN mutation types to ensure the detection limit, sensitivity and stability of the diagnostic method.

Product List

Partial product data

PTEN p.R130Q Reference Standard RQP10119

PTEN p.R130* Reference Standard RQP10120

PTEN p.R130fs*4 Reference Standard RQP10121

PTEN p.R233* Reference Standard RQP10123

PTEN p.T321fs Reference Standard RQP10448

PTEN p.R130Afs*51 Reference Standard RQP10464

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