ECM1 Knockout HeLa Cell Line

The ECM1 Knockout HeLa Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the HeLa human cervical adenocarcinoma cell line. This model features targeted disruption of the ECM1 gene, which encodes extracellular matrix protein 1, a secreted glycoprotein involved in basement membrane organization and integrin-mediated cell adhesion. By ablating ECM1 expression, this cell line enables detailed investigation of ECM1-dependent processes in a well-characterized cancerous epithelial background.

HeLa cells are an immortalized human cervical adenocarcinoma cell line that is positive for human papillomavirus type 18 (HPV18). These cells are widely used in cancer biology research due to their robust growth, well-documented genetic and epigenetic landscape, and the presence of HPV oncoproteins E6 and E7, which inactivate tumor suppressors p53 and Rb. The HeLa background provides a clinically relevant model for studying cervical cancer progression and the interplay between viral oncogenesis and host gene function.

ECM1 is a secreted glycoprotein that interacts with basement membrane components such as perlecan, fibulin-1, collagen IV, and laminin, and binds to cell surface integrin ??1. Through these associations, ECM1 promotes focal adhesion turnover and activates the FAK?CSrc?CAkt signaling axis. ECM1 expression is upregulated by STAT3, NF-??B, TGF-??, and HIF-1??. In turn, ECM1 enhances Wnt/??-catenin signaling and facilitates TGF-??-mediated Smad2/3 activation, leading to the expression of the EMT transcription factor Snail and secretion of matrix metalloproteinase MMP-9. Additionally, ECM1 contributes to VEGF-driven angiogenesis, thus promoting a pro-invasive and pro-metastatic microenvironment.

In cervical adenocarcinoma, ECM1 overexpression correlates with enhanced migration, invasion, and metastatic potential. The HeLa cell line, being HPV18-positive and harboring oncogenic drivers, provides a relevant system to study ECM1 function. The ECM1 Knockout HeLa Cell Line permits dissection of how loss of ECM1 affects integrin-mediated focal adhesion dynamics, EMT transcriptional programming, and MMP-9 secretion. Moreover, this model enables investigation of potential crosstalk between ECM1 and HPV oncoproteins in modulating cytoskeletal reorganization and anoikis resistance.

Researchers can use this cell line in wound healing and Transwell assays to measure cell motility and invasion. Western blot and RT-qPCR allow quantification of EMT markers (Snail, ??-catenin). Immunofluorescence can visualize changes in ECM1 and integrin ??1 localization at focal adhesions, while co-immunoprecipitation identifies disrupted interactions with perlecan, fibulin-1, or collagen IV. RNA-seq analysis reveals global transcriptomic shifts upon ECM1 knockout. This model is also suitable for high-throughput screening to identify ECM1-dependent drug sensitivities. For further information, technical support, or custom gene-editing services, please contact Ascent Research.