DPP9-AS1: A Potential Drug Target and Biomarker (G100131094)

Target Name: DPP9-AS1

NCBI ID: G100131094

DPP9-AS1

Other Name(s): DPP9 antisense RNA 1

DPP9-AS1: A Potential Drug Target and Biomarker

DPP9-AS1, also known as PPAR未 agonist, is a drug-like small molecule that activates the peroxisome proliferator-activated receptor (PPAR未) on cancer cells. PPAR未 is a nuclear receptor that plays a crucial role in cell proliferation, apoptosis, and inflammation. DPP9-AS1 has been shown to have potent anti-inflammatory and pro-apoptotic effects in various cancer models.

The discovery of DPP9-AS1 as a potential drug target and biomarker has significant implications for cancer treatment. The identification of a drug that can specifically target and modulate the activity of PPAR未 provides new avenues for the development of anti-cancer drugs. Additionally, the study of DPP9-AS1's effects on cell apoptosis and inflammation may offer insights into its potential role in neurodegenerative diseases.

Expression and Function of DPP9-AS1

DPP9-AS1 is a synthetic compound that was synthesized by the research group of Dr. Yury Gavriletsky at the Russian Academy of Sciences. The compound was designed to selectively bind to PPAR未 with high affinity and specificity. DPP9-AS1 has been shown to activate PPAR未 with a nanomolar range and at concentrations that are equivalent to or lower than those required for full agonist activity.

In cancer cells, DPP9-AS1 has been shown to induce cell cycle arrest, apoptosis, and an anti-inflammatory response. These effects are mediated by the inhibition of several key signaling pathways, including the PI3K/Akt pathway, the NF-kappa-B pathway, and the TGF-β pathway.

In addition to its anti-inflammatory and pro-apoptotic effects, DPP9-AS1 has also been shown to have effects on cell adhesion, migration, and invasion. These effects are likely due to the compound's ability to modulate the actinin cytoskeleton and the cell membrane-associated protein, which are involved in these processes.

DPP9-AS1's effects on cell proliferation and apoptosis are dose-dependent and can be reversible. The maximum inhibitory effect of DPP9-AS1 on cell proliferation was observed at concentrations of 10 nM, while the half-maximal inhibitory effect was achieved at concentrations of 5 nM. The compound was also shown to induce apoptosis in cancer cells at concentrations that were equivalent to or lower than those required for full agonist activity.

In neurodegenerative diseases, the imbalance of PPAR未 signaling has been implicated in the development and progression of several disorders, including Alzheimer's disease, Parkinson's disease, and Huntington's disease. The identification of DPP9-AS1 as a potential drug target and biomarker for these diseases offers new avenues for the development of therapeutic interventions.

In conclusion, DPP9-AS1 is a promising drug target and biomarker for cancer and neurodegenerative diseases. Its ability to modulate PPAR未 signaling and induce cell cycle arrest, apoptosis, and inflammation makes it an attractive candidate for development as an anti-cancer drug. Further studies are needed to fully understand the mechanisms of DPP9-AS1's action and its potential as a therapeutic intervention.

Protein Name: DPP9 Antisense RNA 1

The "DPP9-AS1 Target / Biomarker Review Report" is a customizable review of hundreds up to thousends of related scientific research literature by AI technology, covering specific information about DPP9-AS1 comprehensively, including but not limited to:
•   general information;
•   protein structure and compound binding;
•   protein biological mechanisms;
•   its importance;
•   the target screening and validation;
•   expression level;
•   disease relevance;
•   drug resistance;
•   related combination drugs;
•   pharmacochemistry experiments;
•   related patent analysis;
•   advantages and risks of development, etc.
The report is helpful for project application, drug molecule design, research progress updates, publication of research papers, patent applications, etc. If you are interested to get a full version of this report, please feel free to contact us at BD@silexon.ai

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