Genome-edited Cells
Large intestine (colon)
The Smurf2 Knockout MC-38 Cell Line is a CRISPR/Cas9-edited murine colon adenocarcinoma model with disruption of the Smurf2 gene. Smurf2 functions as an E3 ubiquitin ligase that negatively regulates TGF-??/BMP signaling by targeting SMAD proteins (SMAD1/2/3/5) and receptors (TGFBR1, BMPR1) for proteasomal degradation. Loss of Smurf2 is expected to enhance SMAD-dependent transcription and signaling output. This knockout cell line is suited for TGF-??/BMP pathway analysis, ubiquitin biology, and colorectal cancer metastasis research. Researchers can utilize Western blotting for phospho-SMADs, SMAD-responsive luciferase reporters, and functional assays such as migration and invasion to dissect Smurf2-dependent mechanisms and pathway crosstalk with Wnt/??-catenin and Hippo signaling.
BCKDHA Knockout HAP1 Polyclonal Cells
Cat. No. ARG22060
FHOD1 Knockout NCI-H1975 Polyclonal Cells
Cat. No. ARG16866
NQO1 Knockout 143B Polyclonal Cells
Cat. No. ARG11782
MORC3 Knockout A549 Polyclonal Cells
Cat. No. ARG10325
NBN Knockout MES-OV Polyclonal Cells
Cat. No. ARG6654
TE-4
Cat. No. ARC0948
The Smurf2 Knockout MC-38 Cell Line is a CRISPR/Cas9-edited knockout cell line engineered to disrupt expression of the Smurf2 gene in the MC-38 murine colon adenocarcinoma background. This loss-of-function model enables precise interrogation of Smurf2-dependent regulatory mechanisms without relying on transient gene silencing approaches. The cell line is provided as a stable knockout and is suitable for a wide range of in vitro applications exploring the molecular consequences of Smurf2 deficiency.
The MC-38 cell line is a well-characterized murine colon adenocarcinoma model originally derived from a chemically induced tumor in C57BL/6 mice. It is widely employed in preclinical oncology research, particularly in studies of colorectal cancer progression, immune checkpoint responses, and tumor microenvironment dynamics. The C57BL/6 genetic background ensures compatibility with syngeneic transplantation models, making this knockout cell line a valuable tool for dissecting tumor-intrinsic signaling pathways in an immunocompetent context.
Smurf2 (SMAD ubiquitylation regulatory factor 2) encodes a HECT-type E3 ubiquitin ligase that negatively regulates TGF-??/BMP signaling by targeting key pathway components for proteasomal degradation. Smurf2 is recruited by the adaptor protein SMAD7 and associates with TGF-?? receptors (TGFBR1) and BMP receptors (BMPR1), directing their ubiquitination and turnover. Additionally, Smurf2 directly ubiquitinates receptor-activated SMAD proteins, including SMAD1, SMAD2, SMAD3, and SMAD5, as well as downstream effectors such as RUNX2 and RhoA. Through these interactions, Smurf2 intersects with related pathways including Wnt/??-catenin signaling, where it interacts with ??-catenin, and Hippo signaling via interaction with YAP. Disruption of Smurf2 is therefore anticipated to relieve negative regulation of SMAD-dependent transcription, leading to sustained or enhanced signaling output upon ligand stimulation.
In the context of MC-38 colorectal cancer cells, Smurf2 knockout provides a model to investigate how elevated TGF-??/BMP pathway activity influences tumor cell behavior. TGF-?? signaling plays dual roles in cancer, acting as a tumor suppressor in early stages and promoting epithelial-mesenchymal transition (EMT), invasion, and metastasis in advanced disease. By ablating a critical negative regulator, this cell line allows researchers to examine consequences on proliferation, migration, invasion, and metastatic potential. Moreover, altered TGF-?? signaling may reshape the tumor microenvironment and modulate responses to immunotherapies, making this model relevant for combination therapy studies.
This knockout cell line is suited for molecular dissection of TGF-??/BMP signaling cascades and ubiquitin-mediated regulatory mechanisms. Researchers can employ phospho-SMAD detection via Western blot or flow cytometry to gauge pathway activation, utilize SMAD-responsive luciferase reporters to quantify transcriptional output, and perform co-immunoprecipitation or proximity ligation assays to map Smurf2 interaction networks. Functional assays such as migration, invasion, and proliferation studies can reveal Smurf2-dependent phenotypes relevant to colorectal cancer metastasis. The cell line also supports investigations into crosstalk with Wnt/??-catenin and Hippo pathways, as well as tumor-immune interactions in syngeneic models. For further technical inquiries, please contact Ascent Research.
