The CCDC90B Knockout HGC-27 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HGC-27 human gastric carcinoma epithelial cell line, in which the CCDC90B gene (also known as MCUR1) has been disrupted to eliminate functional protein expression. This polyclonal pool is generated by CRISPR/Cas9-mediated gene disruption, providing a heterogeneous loss-of-function model suitable for functional studies of CCDC90B in a metastatic gastric cancer context.
HGC-27 is a well-characterized human gastric adenocarcinoma cell line established from the lymph node metastasis of a gastric cancer patient, exhibiting an epithelial phenotype. It serves as a representative model of metastatic gastric adenocarcinoma and is widely employed in gastric cancer research to study tumor biology, metastasis, and drug responses.
CCDC90B (MCUR1) functions as a critical scaffold protein within the mitochondrial calcium uniporter (MCU) complex, where it stabilizes the core components MCU and EMRE (SMDT1) and interacts with the regulatory subunits MICU1 and MICU2. In response to elevated cytosolic Ca2+ concentrations, particularly at endoplasmic reticulum?Cmitochondria contact sites via IP3R?CGRP75?CVDAC1-mediated transfer, CCDC90B facilitates MCU-dependent Ca2+ influx into the mitochondrial matrix. This Ca2+ uptake activates key TCA cycle dehydrogenases, enhancing oxidative phosphorylation and ATP synthesis, while also modulating reactive oxygen species (ROS) homeostasis. Under pathological Ca2+ overload, CCDC90B can promote the opening of the mitochondrial permeability transition pore (mPTP), leading to cytochrome c release and apoptosis.
In the context of HGC-27 gastric carcinoma cells, disruption of CCDC90B offers a valuable loss-of-function model to dissect the role of mitochondrial calcium signaling in cancer metabolism. Given that HGC-27 cells are derived from a metastatic site, this knockout pool is particularly suited to investigate how CCDC90B-dependent Ca2+ flux influences metastatic traits, including cell migration, invasion, and resistance to anoikis. Moreover, as MCU complex activity has been implicated in chemoresistance, this model enables exploration of mitochondrial Ca2+-mediated apoptosis evasion mechanisms frequently observed in gastric cancer.
Typical applications include mechanistic studies of mitochondrial bioenergetics in gastric adenocarcinoma, functional interrogation of the MCU complex through co-immunoprecipitation and live-cell calcium imaging with Rhod-2 AM, and high-throughput chemical screens for MCU modulators. This knockout pool is also suitable for apoptosis profiling using Annexin V/PI staining, mitochondrial membrane potential assessment with TMRE, and metabolic flux analyses to quantify changes in glucose consumption and lactate production. Researchers may employ these cells to validate downstream targets such as MCU, VDAC1, and IP3R, or to assess the impact of CCDC90B loss on ATP production and ROS levels. For additional information or customized gene-edited cell solutions, please contact Ascent Research.
