NUGC-3

Cat.No.: CSC-C7088J

Species: Homo sapiens (Human)

Source: Muscle Metastasis

Morphology: Epithelial

Culture Properties: Adherent

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Cat.No.
CSC-C7088J
Description
established from brachialis muscle metastasis of a 72-year-old male patient with gastric adenocarcinoma
Species
Homo sapiens (Human)
Source
Muscle Metastasis
Recommended Medium
90% RPMI 1640 + 10% FBS
Culture Properties
Adherent
Morphology
Epithelial
Application
Cancer research
Size
1 Frozen Vial
Disease
Gastric Adenocarcinoma
Storage
Directly and immediately transfer cells from dry ice to liquid nitrogen upon receiving and keep the cells in liquid nitrogen until ready for use.
Shipping
Dry Ice
Restricted Use
For research use only. Not for use in diagnostic procedures.
Quality Control
All cells test negative for mycoplasma, bacteria, yeast, and fungi.
BioSafety Level
BSL-1
Synonyms
NUGC3; NU-GC-3
Metastatic Site
Brachialis muscle
Citation Guidance
If you use this products in your scientific publication, it should be cited in the publication as: Creative Bioarray cat no. If your paper has been published, please click here to submit the PubMed ID of your paper to get a coupon.

The NUGC-3 cell line is a human-derived epithelial model established from a metastatic lymph node of a patient with gastric adenocarcinoma (GC). It represents a poorly differentiated (or diffuse-type) subtype according to the Lauren classification, which is often associated with aggressive behavior, early metastasis, and a less favorable prognosis compared to the intestinal-type. As a cell line derived from a metastatic site, NUGC-3 inherently models the advanced, disseminated stage of the disease, providing a critical tool for studying the mechanisms underlying gastric cancer progression and therapeutic resistance.

NUGC-3 cells exhibit an adherent, epithelial-like morphology in culture, though they may display a somewhat scattered growth pattern consistent with diffuse-type characteristics. A key molecular feature is its reported microsatellite instability-high (MSI-H) status, resulting from deficient DNA mismatch repair (dMMR). This genetic trait leads to a high tumor mutational burden (TMB), which has significant implications for the tumor's biological behavior and its potential response to immunotherapy. NUGC-3 is tumorigenic in immunocompromised mice, capable of forming tumors in vivo, and it generally retains a wild-type status for the TP53 gene, distinguishing it from many other GC models that harbor TP53 mutations.

The Expression and Role of TMEM176B in Gastric Cancer Cells

This study investigated the role of the differentially expressed gene TMEM176B in gastric cancer (GC). Western blotting and qPCR analysis were used to assess TMEM176B expression in normal human gastric mucosa cells (GES-1) and human GC cell lines (BGC-823 and NUGC-3). shRNA-mediated TMEM176B knockdown in cancer cells was used for phenotypic analysis, proliferation assays, and apoptosis experiments.

The results indicated that TMEM176B was highly expressed in GC cell lines. TMEM176B knockdown in GC cell lines inhibited cell proliferation (reduced CCK8 and colony formation), increased apoptosis (higher Bax/Bcl2 ratio), and arrested the cell cycle in the G0/G1 phase. This identified TMEM176B's role in GC development and progression, offering molecular targets and a foundation for future treatments.

Analysis of normal human gastric mucosa cells (GES-1) and human GC cell lines (BGC-823 and NUGC-3) revealed significantly higher TMEM176B expression in BGC-823 and NUGC-3 cells than in GES-1 cells.

Fig. 1. TMEM176B was highly expressed in BGC-823 and NUGC-3 cells (Jiang, Zhenhua, et al., 2025).

Knockdown of TMEM176B significantly reduced the growth rate of BGC-823 (a) and NUGC-3 cells (b). EdU assays showed that TMEM176B knockdown significantly inhibited the proliferation of BGC-823 cells compared to the shNC group (c). A similar inhibitory effect on proliferation was observed in NUGC-3 cells (d).

Fig. 2. Knockdown of TMEM176B inhibited the growth rate and proliferative capacity of gastric cancer cells (Jiang, Zhenhua, et al., 2025).

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