College
College of Arts and Sciences
Mentor Information
Dr. Stuart Maudsley
Description
Synthetic promoters and chemogenetics offer emerging strategies to control cancer cell signaling. Prior work examined tumor-specific promoters and glutamatergic signaling in cancer, yet evidence remains limited on restricting DREADD-engineered GPCRs to tumor cells using multi-gene circuits, particularly across age groups. This review evaluates synthetic promoter–gene circuit designs enabling tumor-restricted expression of DREADD-modified mGluR2 and assesses age-related effects on performance. A comprehensive review of 54 peer-reviewed articles was conducted, investigating factors such as relations between age and changes in gene expression, epigenetic promoter alterations within cancer therapies, and mGluR2 function and implications for therapeutic applications in cancer therapies and immunotherapy. Articles were selected through scientific databases, such as USF Library, PubMed, ScienceDirect, and SemanticScholar through the use of key words: “synthetic promoter,” “mGluR2,” “DREADD,” and “gene circuits.” Synthetic promoters paired with RNA-based circuits enabled tumor-selective gene expression by integrating tumor-specific transcriptional and microRNA signals. DREADD-modified mGluR2 can regulate glutamatergic signaling in cancer cells and placing it under tumor-selective promoters confines chemogenetic control to malignant tissue. LY341495 (mGluR2/3 antagonist) studies show that inhibiting mGluR2/3 reduces tumor growth by targeting suppressor cells and altering tumor microenvironments. Older patients responded less effectively than pediatric groups, likely due to reduced promoter activity with age. Engineered promoters and RNA circuits can safely restrict DREADD-mGluR2 expression to tumors, supporting potential chemogenetic targeting of glutamate pathways. Gaps remain of course, including testing across multiple cancer models and confirming safe ligand control. Further research should evaluate how DREADD-mGluR2 activation affects tumor immunity in vivo across age groups.
Engineering Synthetic Promoters and Gene Circuits for Tumor-Specific DREADD- mGluR2 Expression Across Age Groups
Synthetic promoters and chemogenetics offer emerging strategies to control cancer cell signaling. Prior work examined tumor-specific promoters and glutamatergic signaling in cancer, yet evidence remains limited on restricting DREADD-engineered GPCRs to tumor cells using multi-gene circuits, particularly across age groups. This review evaluates synthetic promoter–gene circuit designs enabling tumor-restricted expression of DREADD-modified mGluR2 and assesses age-related effects on performance. A comprehensive review of 54 peer-reviewed articles was conducted, investigating factors such as relations between age and changes in gene expression, epigenetic promoter alterations within cancer therapies, and mGluR2 function and implications for therapeutic applications in cancer therapies and immunotherapy. Articles were selected through scientific databases, such as USF Library, PubMed, ScienceDirect, and SemanticScholar through the use of key words: “synthetic promoter,” “mGluR2,” “DREADD,” and “gene circuits.” Synthetic promoters paired with RNA-based circuits enabled tumor-selective gene expression by integrating tumor-specific transcriptional and microRNA signals. DREADD-modified mGluR2 can regulate glutamatergic signaling in cancer cells and placing it under tumor-selective promoters confines chemogenetic control to malignant tissue. LY341495 (mGluR2/3 antagonist) studies show that inhibiting mGluR2/3 reduces tumor growth by targeting suppressor cells and altering tumor microenvironments. Older patients responded less effectively than pediatric groups, likely due to reduced promoter activity with age. Engineered promoters and RNA circuits can safely restrict DREADD-mGluR2 expression to tumors, supporting potential chemogenetic targeting of glutamate pathways. Gaps remain of course, including testing across multiple cancer models and confirming safe ligand control. Further research should evaluate how DREADD-mGluR2 activation affects tumor immunity in vivo across age groups.
