The CD164 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population with disruption of the CD164 gene. The polyclonal format provides a heterogeneous pool of gene-edited cells reflecting average loss-of-function effects across the population. This model enables robust functional assays without viral transduction or siRNA.
HeLa cells, derived from cervical adenocarcinoma, are widely used in cancer research for studies of proliferation, migration, and signaling. Their robust growth and genetic stability make them an ideal host for generating gene knockouts. The CD164 knockout HeLa polyclonal cells retain epithelial morphology and growth properties of the parental line while offering a consistent knockout background for comparative studies.
CD164 is a type I integral membrane sialomucin that functions as a cell adhesion molecule and hematopoietic stem cell homing regulator. It signals downstream of CXCL12/SDF-1 through interaction with CXCR4 and syntenin-1 (SDCBP). CD164 activity promotes migration and proliferation via RhoA and mTORC1, and influences cell cycle progression through p21 and CDK inhibitors. It also interacts with CD63 and is regulated by inflammatory cytokines and growth factors, integrating extracellular cues to control motility and growth.
In HeLa cervical cancer cells, CD164 knockout impairs CD164-mediated adhesion and CXCR4 signaling. Loss of CD164 attenuates migration and proliferation by disrupting RhoA and mTORC1 pathways, and may alter cell cycle regulation through reduced p21, diminishing tumorigenic properties. This polyclonal knockout model enables interrogation of CD164 contributions to cancer cell behavior, metastasis, and chemokine responses, highlighting potential therapeutic targets.
Research applications include cancer cell migration assays (Boyden chamber, wound healing), CXCR4 signaling analysis by flow cytometry, adhesion and metastasis assays, and hematopoietic stem cell biology studies. Downstream effects can be confirmed via Western blot for mTORC1 and p21, proliferation (MTT) assays, and adhesion assays. This system facilitates dissection of CD164-dependent signaling in cancer and hematopoietic disorders. For additional information, contact Ascent Research.
