NUGC-3
Cat.No.: CSC-C7088J
Species: Homo sapiens (Human)
Source: Muscle Metastasis
Morphology: Epithelial
Culture Properties: Adherent
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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.


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