The DUSP23 knockout HGC-27 polyclonal cell product is a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human gastric adenocarcinoma cell line HGC-27. This loss-of-function model is generated through CRISPR/Cas9-mediated gene disruption of the DUSP23 locus, resulting in a heterogeneous pool of cells with targeted variations in the DUSP23 gene. The polyclonal format provides a biologically relevant system for studying the functional consequences of DUSP23 deficiency within a genetically diverse cell pool, capturing a range of knockout-related phenotypes without the bottleneck imposed by single-cell cloning. The product is supplied as a live cell population suitable for immediate expansion and downstream functional analyses in cancer biology research.
HGC-27 is an adherent epithelial cell line originally established from the lymph node metastasis of a human gastric adenocarcinoma, serving as a well-characterized model for studying advanced gastric cancer biology. As a metastatic derivative, HGC-27 retains key features of aggressive gastric tumors, including deregulated growth signaling, invasive capacity, and altered drug sensitivity. This cell line is widely used to investigate the molecular mechanisms underlying gastric cancer progression, metastasis, and therapeutic resistance, making it an appropriate host for interrogating the tumor-suppressive or oncogenic roles of signaling regulators such as DUSP23 in a disease-relevant context.
DUSP23 encodes a dual-specificity phosphatase that functions as a negative regulator of mitogen-activated protein kinase (MAPK) signaling by dephosphorylating key MAPK effectors. Within the MAPK cascade hierarchy, DUSP23 directly interacts with and inactivates ERK1/2, JNK, and p38 MAPKs, thereby dampening signal propagation downstream of mitogenic stimuli and cellular stress inputs. Its activity is tightly linked to classic MAPK pathway components, including RAS, RAF, and MEK, which transmit upstream signals to ERK, JNK, and p38 modules. DUSP23 is itself regulated by MAPK signaling, positioning it within a negative-feedback loop that modulates the magnitude and duration of pathway activation. This regulatory node is critical for maintaining signaling homeostasis, and loss of DUSP23 function perturbs the balance between kinase-driven oncogenic signals and phosphatase-mediated tumor-suppressive constraints.
In HGC-27 gastric cancer cells, DUSP23 knockout is anticipated to unleash sustained MAPK pathway activation, a hallmark of aggressive malignancies. Hyperphosphorylation of ERK1/2, JNK, and p38 resulting from DUSP23 loss can drive transcriptional programs orchestrated by immediate-early genes and downstream transcription factors, fostering proliferation, survival, migration, and drug resistance. The polyclonal knockout population mirrors the heterogeneity of pathway activation states seen in clinical tumors, providing a robust platform to dissect how DUSP23 deficiency reprograms signaling networks and contributes to oncogenic phenotypes within a metastatic gastric cancer background. This model is particularly pertinent for exploring DUSP23??s role in gastric cancer, as well as in related gastrointestinal malignancies and other cancers where MAPK hyperactivation is a driver event.
Researchers can employ this DUSP23 knockout polyclonal cell model across a spectrum of functional assays, including western blotting to assess phospho-ERK1/2, phospho-JNK, and phospho-p38 levels, providing direct readouts of MAPK pathway activity. RT-qPCR quantitation of immediate-early gene induction (e.g., FOS, JUN) can measure transcriptional responses downstream of unchecked MAPK signaling. The cells are well-suited for migration and invasion assays to evaluate metastatic potential, apoptosis assays to determine cell death susceptibility, and drug sensitivity analyses to probe resistance mechanisms in gastric cancer. This product enables robust interrogation of tumor progression pathways, signal transduction networks, and therapeutic vulnerabilities associated with DUSP23 deficiency. For additional technical specifications or ordering information, please contact Ascent Research.
