The DMXL1 Knockout MES-OV Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the MES-OV ovarian carcinoma cell line. This product contains a heterogeneous pool of cells with targeted DMXL1 gene disruptions, generated via CRISPR/Cas9-mediated editing. As a non-clonal pool, it circumvents clonal artifacts and provides a robust loss-of-function model for studying DMXL1-dependent processes in an epithelial ovarian cancer context, suitable for functional genomics and mechanistic investigations.
The MES-OV cell line, established from a human ovarian carcinoma, exhibits features of high-grade serous adenocarcinoma. This adherent epithelial model retains oncogenic signaling and autophagic activity relevant to advanced ovarian tumors. Its native cellular context supports studies of lysosomal function and tumor progression, making it an ideal host for gene disruption. MES-OV is widely used to explore mechanisms of ovarian cancer growth, metastasis, and drug resistance.
DMXL1 functions as a scaffold protein critical for vacuolar H+-ATPase (V-ATPase) assembly, interacting with ATP6V1A, ATP6V0D1, and the LAMTOR/Ragulator complex. It facilitates endolysosomal acidification and is essential for autophagy and mTORC1 signaling. Regulated by mTORC1 and nutrient availability, DMXL1 controls lysosomal pH, autophagic flux, and mTORC1 localization. The protein cooperates with RAB7 in vesicular trafficking and influences degradation of LC3-II and p62. Thus, DMXL1 integrates stress signals to manage lysosomal degradation and cellular metabolism.
In ovarian cancer, elevated V-ATPase activity supports tumor survival and chemoresistance. DMXL1 knockout in MES-OV cells models V-ATPase dysfunction, leading to impaired lysosomal acidification, blocked autophagy, and mTORC1 dysregulation. This perturbation can affect tumor cell metabolism and increase cisplatin sensitivity. The model enables focused dissection of the DMXL1?CV-ATPase axis in ovarian cancer progression, providing insight into lysosomal contributions to malignancy and potential therapeutic targets.
This polyclonal knockout product is applicable to a range of assays, including western blotting for V-ATPase subunits, LC3-II, and p62; immunofluorescence for LAMP1 and LC3; LysoTracker staining; autophagy flux analysis; and phospho-S6K measurement for mTORC1 activity. Co-immunoprecipitation assesses V-ATPase complex integrity, and proliferation or cisplatin sensitivity assays evaluate cancer-relevant endpoints. These tools support research into endolysosomal biology, drug resistance, and mTOR signaling in ovarian cancer. For further details, contact Ascent Research.
