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T3M-4

Cat.No.: CSC-C6425J

Species: Human

Morphology: epithelial-like

Culture Properties: Adherent cells

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Cat.No.
CSC-C6425J
Description
Pancreatic adenocarcinoma producing CEA. K-ras activated. Cell growth is slow.
Species
Human
Tissue of Origin
pancreas, lymph node meta
Recommended Medium
HamF10 + 10% h.i. FBS
Culture Properties
Adherent cells
Morphology
epithelial-like
Storage and Shipping
Ship in dry ice.
Store in liquid nitrogen.
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 T3M-4 cell line was established in 1986 from a lymph node metastasis of a patient with pancreatic ductal adenocarcinoma (PDAC), the most common and aggressive type of pancreatic cancer. The cell line has a typical epithelial morphology and carries key genetic mutations commonly seen in PDAC, including mutations in KRAS (G12V) and TP53. T3M-4 cells are characterized by their high tumorigenicity and metastatic potential in immunodeficient mice, consistent with their metastatic origin. They also express relevant biomarkers, such as CA19-9, and retain the ability to interact with the desmoplastic stroma, a hallmark feature of pancreatic tumors.

T3M-4 has been widely used to study key aspects of PDAC, particularly invasion, metastasis, and therapeutic resistance. Its high clinical relevance, robust in vivo growth and metastasis formation, retention of desmoplastic reaction capabilities in co-culture or xenograft models, and its utility as a model for intrinsic and acquired chemoresistance, provide a representative platform for investigating this lethal cancer. Researchers leverage T3M-4 to test novel therapeutics, including chemotherapy combinations, targeted agents (especially against KRAS downstream pathways, EGFR, and MEK), and drugs aimed at disrupting the tumor-stroma interactions (e.g., Hedgehog inhibitors or FAK inhibitors). The availability of T3M-4 cells allows for reproducible and consistent experimental results, contributing to the advancement of pancreatic cancer research and the development of more effective treatment options.

LAT1 is Expressed on Exosomes Isolated from Cell Culture Supernatant of T3M-4 Cells

L-type amino acid transporter 1 (LAT1) is upregulated in various cancers and contributes to the growth and proliferation of cancer cells. Previous clinicopathological studies have revealed associations between the high expression of LAT1 and the poor prognosis in multiple cancer types. However, in those studies, LAT1 expression was assessed only by immunohistochemistry on resected tumors or tissue biopsies. Cancer cell-derived exosomes are gaining increasing attention as a resource of diagnostic, prognostic, and therapeutic biomarkers. In this study, we revealed the expression of LAT1 on exosomes from pancreatic cancer T3M-4 cells by western blotting, immunoprecipitation, and immuno-transmission electron microscopy. The results showed that LAT1 was expressed on exosomes secreted by T3M-4 cells into the cell culture supernatant.

The expression of LAT1 on exosomes isolated from T3M-4 cell culture supernatant.Fig. 1. Detection of LAT1 in exosome fraction isolated from T3M-4 cell culture supernatant (Liu, Yumiao, et al. 2024).

Gemcitabine Increases HLA-I Expression by Pancreatic Cancer Cells

Pancreatic cancer is a deadly disease with a five-year overall survival rate of only 13%. Therefore, the existing treatment methods needs to be adjusted, with attention shifting towards liberating the stalled efficacy of immunotherapies. Select chemotherapeutic agents with inherent immune-modifying behaviors could revitalize immune activity against pancreatic tumors and potentiate immunotherapeutic success. In this study, Larson, Alaina C., et al. characterized the influence of gemcitabine, a chemotherapeutic agent approved for the treatment of pancreatic cancer, on tumor antigen presentation by human leukocyte antigen class I (HLA-I). Gemcitabine increased pancreatic cancer cells' HLA-I mRNA transcripts, total protein, surface expression, and surface stability. These data support further exploration of immunotherapies, including peptide-based vaccines, to be used with gemcitabine as new combination treatment modalities for pancreatic cancer.

Pancreatic cancer cell lines were treated with gemcitabine at varying concentrations for 48 h and mRNA levels were assessed via qRT-PCR.Fig. 2. HLA-I mRNA transcripts are enhanced by gemcitabine (Larson, Alaina C., et al. 2024)

S2-013, T3M-4, and PANC-1 cells were treated with various concentrations of gemcitabine for 72 h. Western blot analysis monitored changes in total protein levels of HLA-I components.Fig. 3. Gemcitabine augments protein expression of HLA-I (Larson, Alaina C., et al. 2024).

Are tumor stem cells being targeted in clinical trials?

Yes, targeting tumor stem cells is an active area of investigation in clinical trials. Several trials are evaluating the effectiveness of therapies designed to specifically target and eliminate tumor stem cells.

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Average Rating: 5.0    |    1 Scientist has reviewed this product

Well characterized

These cells were well characterized and matched the description provided by Creative Bioarray.

19 Jan 2023


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