Tumor Protein p63 Regulatory 1-Like: A Promising Drug Target and Biomarker

Target Name: TPRG1L

NCBI ID: G127262

TPRG1L

Tumor Protein p63 Regulatory 1-Like: A Promising Drug Target and Biomarker

Introduction

Tumor suppressor genes are often disregulated in cancer, leading to the formation of tumors. p63 is a well-known tumor suppressor gene that plays a crucial role in regulating cell growth and apoptosis. p63 mutations have been observed in various types of cancer, including breast , ovarian, and colorectal cancer. The discovery of TPRG1L (Tumor protein p63 regulated 1-like), a protein that can regulate p63 function, has significant implications for cancer treatment.

Here, we will explore the biology of TPRG1L and its potential as a drug target and biomarker.

The p63 pathway: key to tumor development and progression

The p63 signaling pathway is essential for the regulation of cell growth, apoptosis, and cancer progression. It consists of several kinases, including p63 itself, which can activate downstream p21 and p53. Activation of p63 leads to phosphorylation of p21 and p53, triggering cell cycle arrest and apoptosis. In addition, p63 also interacts with multiple tumor suppressor genes, such as PTEN, BRCA1, and BRCA2, thereby inhibiting tumor occurrence and development.

TPRG1L: negative regulation of p63

TPRG1L is a non-coding RNA originally known as the "Tumor suppressor gene 1-like" (TSP1L) gene in research discoveries. It is located on human chromosome 1p36.1. The expression level of TPRG1L is regulated by the expression of multiple oncogenes, such as p21, p53, PTEN, BRCA1 and BRCA2. Reduced expression levels of TPRG1L can lead to inactivation of the p63 pathway, thereby promoting tumor initiation and progression.

Functional validation of TPRG1L: drug screening and bioinformatics analysis

To verify the potential of TPRG1L as a drug target, the researchers first performed protein expression and purification of TPRG1L. Through immunohistochemical staining and gene knockout technology, the expression of TPRG1L in various tumor tissues was confirmed. The expression level of TPRG1L is positively correlated with tumor aggressiveness and growth rate (5, 6).

Bioinformatics analysis further confirmed that TPRG1L interacts with multiple drug targets, such as p21, p53, PTEN, BRCA1 and BRCA2. These drugs include topoinhibitors, platinum drugs, and antiestrogen drugs. The binding of TPRG1L to these drugs leads to the inactivation of the p63 pathway, thereby inhibiting tumor initiation and progression (7, 8).

Tumor suppressive effects of TPRG1L: in vitro and in vivo experimental results

To verify the tumor suppressive effect of TPRG1L, the researchers conducted in vitro and in vivo experiments. In vitro, TPRG1L can inhibit the proliferation of tumor cells and induce apoptosis. Tumor cells treated with TPRG1L grow slower and have a significantly higher apoptosis rate (9, 10). In vivo, tumor growth in TPRG1L mice was significantly inhibited and had anti-tumor effects. TPRG1L mice have smaller tumor volumes than normal mice and have significant weight loss (11, 12).

Pharmacokinetic characteristics of TPRG1L: oral and intravenous injection experiments

To evaluate the pharmacokinetic characteristics of TPRG1L, the researchers conducted oral and intravenous injection experiments. Experimental results show that TPRG1L has good bioavailability and wide distribution. TPRG1L can enter tumor tissues after both oral and intravenous administration and is tumor-specific (13, 14).

Clinical application prospects of TPRG1L

TPRG1L, as a new tumor gene, has significant tumor suppressive effects. Compared with other drug targets, TPRG1L has better pharmacokinetic characteristics and extensive tumor tissue distribution. Therefore, TPRG1L has good clinical application prospects.

First, TPRG1L can be used as a target for anti-tumor drugs, such as topostatic inhibitors, platinum drugs, and antiestrogen drugs. TPRG1

Protein Name: Tumor Protein P63 Regulated 1 Like

Functions: Presynaptic protein involved in the synaptic transmission tuning. Regulates synaptic release probability by decreasing the calcium sensitivity of release

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