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Home / Products / Genome-edited Cells / Knockout Cell Lines / CCM2 Knockout A549 Polyclonal Cells

Cat. No. ARG43208

CCM2 Knockout A549 Polyclonal Cells

Product Type:
Polyclonal Cell Population
Species:
Homo sapiens (Human)
Tissue Source:
Lung
Disease:
Lung adenocarcinoma

Datasheet

CRISPR/Cas9-edited polyclonal knockout cell population derived from AGS human gastric adenocarcinoma cells with targeted disruption of the CCM2 gene. CCM2 encodes a scaffold protein of the CCM complex that maintains cell junction integrity by suppressing RhoA/ROCK and MEKK3/ERK signaling. Loss of CCM2 leads to RhoA hyperactivation, disrupted E-cadherin/??-catenin localization, and enhanced EMT-associated migration. This model is ideal for studying gastric cancer cell junction dynamics, Rho/ROCK and MAPK/ERK pathway crosstalk, and the CCM complex in epithelial biology. Representative assays include western blotting, immunofluorescence, RhoA activation assay, wound healing, and TEER measurement. Contact Ascent Research for more information.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice

Disclaimer:

For Research Use Only

Characteristics

Host Cell

A549

Sex of Donor

Male

Age

58 years

Derived From Site

Lung

Gene Name

CCM2

Gene Identifier

NCBI Gene ID 83605

Storage

Liquid nitrogen (LN2)
Culture Conditions

Growth medium

MEM

Supplement(s)

10% Fetal Bovine Serum, 1% Penicillin-Streptomycin Solution

Temperature

37°C

Atmosphere

5% CO₂
Quality Control

Sterility testing

The bacterial, yeast, and fungi are not detected in these cells by daily monitor.

Mycoplasma testing

Negative for mycoplasma through PCR analysis
Disclaimer

Intended Use

This product is intended for laboratory in vitro use only. lt is not intended for diagnostic, therapeutic, or clinical applications.

Disclaimer

Ascent Research endeavors to provide accurate and up-to-date product information. However, no warranties or representations are made regarding its completeness or reliability. References to scientific literature and patents are for informational purposes only, and the customer assumes sole responsibility for verifying their accuracy.

By accepting this product, the customer acknowledges and agrees to assume all risks associated with its receipt, handling, storage, disposal, and use, including compliance with all applicable safety and environmental regulations and precautions. Relevant laws, regulations, and ethical guidelines must be followed in conducting any research, modifications, or derivatives derived from this product.

This product is provided "AS IS", and except as expressly stated herein, Ascent Research disclaims all other warranties, express or implied. Under no circumstances shall Ascent Research, its affiliates, or representatives be liable for indirect, incidental, consequential, or punitive damages arising from the use of this material. While Ascent Research employs rigorous quality control measures, we shall not be held responsible for damages resulting from misidentification or misinterpretation of the provided materials.

Description

The CCM2 Knockout AGS Polyclonal Cells are a CRISPR/Cas9-engineered polyclonal population of human gastric adenocarcinoma (AGS) cells with targeted disruption of the CCM2 gene. This loss-of-function model eliminates the CCM2 scaffold protein, enabling dissection of junctional integrity, RhoA/ROCK, and MEKK3/ERK signaling in a gastric epithelial background.

The AGS cell line originates from a poorly differentiated gastric adenocarcinoma and is a classic model for studying gastric cancer cell biology, including adhesion, migration, and epithelial?Cmesenchymal transition (EMT). Its epithelial origin and tumorigenic properties make it ideal for interrogating the role of cell?Ccell junction regulators such as CCM2 in gastric carcinogenesis and metastatic progression.

CCM2 serves as a core scaffold of the CCM complex, binding KRIT1 (CCM1) and PDCD10 (CCM3) to stabilize adherens and tight junctions. It negatively regulates RhoA/ROCK and MEKK3/ERK1/2 pathways downstream of integrin ??1 and ICAP1. CCM2 loss leads to hyperactivation of RhoA, driving ROCK-mediated actin stress fiber formation, and to MEKK3-driven ERK1/2 phosphorylation, which disrupts E-cadherin/??-catenin complexes and promotes junction disassembly. Interactions with SMURF1 further link CCM2 to ubiquitin-dependent RhoA control.

In AGS cells, CCM2 knockout recapitulates junctional defects, enhanced migration, and EMT-like phenotypes, making the model directly relevant to gastric cancer pathology. The polyclonal feature captures heterogeneous knockout effects, reflecting in vivo tumor cell diversity and providing robustness for pharmacological intervention studies aiming to restore junction integrity or inhibit Rho/ROCK and MAPK/ERK cascades.

Applications include western blot analysis of CCM2, E-cadherin, and phospho-ERK; immunofluorescence for ??-catenin, ZO-1, and F?actin; RhoA GTPase activation assays; wound healing and transwell invasion assays; and TEER measurement for barrier function. The cells support mechanistic studies of CCM signaling, drug testing to normalize ROCK/ERK hyperactivity, and angiogenesis research. For additional details, please contact Ascent Research.