Introducing GPR171 Knockout LoVo Polyclonal Cells as a CRISPR/Cas9-edited polyclonal knockout cell population derived from the LoVo human colorectal adenocarcinoma line. This product provides a loss-of-function model for studying GPR171, a G protein-coupled receptor involved in immune checkpoint regulation and energy homeostasis. The polyclonal format ensures genetic heterogeneity, reflecting population-level gene disruption and enabling robust functional genomics studies without the limitations of single-cell clones.
The LoVo cell line was established from a lymph node metastasis of a 56-year-old Caucasian male with Dukes’ type C colorectal adenocarcinoma. LoVo cells harbor well-characterized driver mutations, including APC, KRAS, and TP53, making them a representative model for metastatic colorectal cancer. Their epithelial origin and metastatic phenotype render them suitable for investigating tumor cell-intrinsic signaling pathways and interactions with the immune microenvironment.
GPR171 encodes a receptor for the proSAAS-derived neuropeptide BigLEN. Upon ligand binding, GPR171 couples to Gi/o proteins to inhibit adenylyl cyclase, thereby reducing intracellular cAMP levels and attenuating protein kinase A (PKA) activity. This signaling cascade further involves downstream effectors such as SHP-2 and contributes to the upregulation of immune checkpoint markers including PD-1 and TIM-3. Interacting partners include Gi/o proteins, ??-arrestins, and G protein-coupled receptor kinases (GRKs), which regulate receptor desensitization and trafficking. In immune cells, GPR171 activation promotes T cell exhaustion, facilitating immune evasion; however, its role in colorectal cancer cells themselves remains an area of active investigation.
In colorectal cancer, GPR171-mediated pathways may support tumor immune escape, linking neuropeptide signaling to cancer immunology. The LoVo colorectal adenocarcinoma model, with its defined mutational background, allows dissection of GPR171 function in epithelial cancer cells and their crosstalk with immune components. By employing this knockout pool, researchers can interrogate how loss of GPR171 alters cAMP signaling, downstream transcriptional programs, and surface expression of immune modulatory molecules, thereby assessing its contribution to tumor progression and immune surveillance.
These polyclonal knockout cells are well-suited for a variety of experimental approaches, including western blotting to confirm target protein depletion, RT-qPCR to assess transcriptional changes, flow cytometry for surface marker analysis, and cAMP assays to quantify second messenger levels. Co-immunoprecipitation studies can probe protein?Cprotein interactions involving Gi/o proteins or ??-arrestins, while migration and invasion assays evaluate metastatic potential. Drug sensitivity analyses may reveal altered responses to chemotherapeutics or immunomodulators. For further information or technical support, please contact Ascent Research.
