In Stock Cell Lines
Homo sapiens (Human)
Breast (mammary gland)
Adherent
The SLC26A9 Knockout MDA-MB-231 Cell Line is a CRISPR/Cas9-edited knockout cell line generated from MDA-MB-231 triple-negative breast cancer cells, featuring targeted disruption of the SLC26A9 gene. This model provides a defined loss-of-function tool for investigating the roles of SLC26A9-mediated chloride/bicarbonate exchange and pH regulation in cancer cell biology. SLC26A9 is a regulated anion exchanger that interacts with CFTR and SLC26A6, and its knockout in the metastatic, TP53-mutant background of MDA-MB-231 enables studies of ion transporter-dependent migration and invasion. Ideal for applications in drug discovery, ion transport assays, and CFTR-SLC26A9 pathway analysis.
COMMD7 Knockout HT29 Polyclonal Cells
Cat. No. ARG14310
KRTCAP2 Knockout Raji Polyclonal Cells
Cat. No. ARG23954
GSN Knockout NCI-H1975 Polyclonal Cells
Cat. No. ARG31579
DNMT3A Knockout Lovo Polyclonal Cells
Cat. No. ARG39445
E2F4 Knockout HAP1 Polyclonal Cells
Cat. No. ARG40249
PDXK Knockout HEK293T Polyclonal Cells
Cat. No. ARG3815
The SLC26A9 Knockout MDA-MB-231 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the MDA-MB-231 human breast adenocarcinoma cell line, featuring targeted disruption of the SLC26A9 gene. This loss-of-function model enables dissection of SLC26A9-dependent anion transport and signaling without altering the endogenous genetic background of the parental line. The cell line serves as a robust platform for studying chloride/bicarbonate exchange mechanisms and their influence on cancer cell physiology.
MDA-MB-231 is a triple-negative breast cancer (TNBC) cell line with mesenchymal-like characteristics, isolated from the pleural effusion of a patient with invasive ductal carcinoma. It harbors a TP53 mutation, exhibits high metastatic potential, and is widely employed in cancer biology and metastasis research. Its aggressive phenotype and defined ion channel expression profile make it a suitable host for examining the role of SLC26A9 in oncogenic processes.
SLC26A9 encodes an electroneutral Cl?/HCO3? exchanger that is regulated by CFTR, cAMP/PKA, WNK kinases, and IL-13. It interacts with CFTR, SLC26A6, SLC26A3, PDZK1, and NHERF1 to modulate chloride and bicarbonate secretion, thereby controlling intracellular pH and cell volume. Within the CFTR-mediated ion transport pathway, SLC26A9 functions alongside WNK1, SPAK, and NBCe1, linking cAMP/PKA signaling to epithelial fluid secretion and pH homeostasis. Disruption of SLC26A9 in this cellular context is expected to perturb these interconnected ion-regulatory networks.
In MDA-MB-231 cells, SLC26A9 knockout disrupts anion homeostasis and may impair pH-dependent signaling, potentially affecting migratory and invasive properties critical to TNBC progression. The mesenchymal-like nature and TP53 mutant background of the host line render it an informative model for investigating how aberrant ion transport drives tumor malignancy. This knockout cell line enables direct assessment of SLC26A9’s contribution to cancer cell behavior, including migration and invasion, under physiologically relevant conditions.
Researchers can utilize this cell line for mechanistic studies of ion transporters in breast cancer, drug discovery targeting anion exchangers, and functional interrogation of CFTR-SLC26A9 interactions. Typical assays include intracellular pH measurements using BCECF, ion transport assays, wound healing migration assays, Transwell invasion assays, as well as molecular validation by Western blotting, RT-qPCR, and immunofluorescence. For further technical details, please contact Ascent Research.
