UT-7
Cat.No.: CSC-C0294
Species: Homo sapiens (Human)
Source: Bone Marrow
Morphology: round (relatively large) cells growing singly in suspension
Culture Properties: Suspension
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Immunology: CD3 -, CD4 -, CD13 +, CD14 -, CD15 -, CD19 -, CD33 +, CD34 -, CD41 (+), CD42 (+), CD68 +, CD235a (+), HLA-DR (+)
Viruses: ELISA: reverse transcriptase negative
UT-7 is a well-characterized human acute myeloid leukemia cell line established in 1988 from the bone marrow of a 64-year-old male patient with acute megakaryoblastic leukemia. The cells exhibit round morphology, grow predominantly in suspension with approximately 1–2% slight adherence, and possess a hypotetraploid karyotype with extensive subclonal variation.
The defining and most valuable feature of UT-7 is its absolute cytokine dependence for growth and survival. The cells are strictly dependent on interleukin-3 (IL-3), granulocyte-macrophage colony-stimulating factor (GM-CSF), or erythropoietin (EPO). This stringent factor dependency renders UT-7 an exceptionally sensitive and quantitative bioassay system for these hematopoietic growth factors.
UT-7 exhibits bipotential differentiation capacity. It can be induced to differentiate along either the erythroid pathway (by EPO) or the megakaryocytic pathway (by phorbol myristate acetate). This plasticity has enabled the derivation of specialized sublines—UT-7/Epo (EPO-dependent), UT-7/GM (GM-CSF-dependent), and UT-7/TPO (thrombopoietin-dependent)—each serving as tailored models for studying specific hematopoietic lineages and signaling pathways.
CD81 Knockdown Inhibits Proliferation and Inducts Apoptosis of AMKL cell line UT-7
CD81 is a cell surface protein that plays an important part in tumor progression. Several studies have shown that CD81 is crucial for cancer cell proliferation, invasion, and metastasis, particularly in leukemia. Su, Narun and Xiaohao Hu hypothesized that CD81 might play a vital role in acute megakaryoblastic leukemia (AMKL). They constructed CD81 knockdown cell line using shRNA and found that CD81 knockout can inhibit the proliferation of AMKL and increase the apoptosis of AMKL in vitro. Therefore, CD81 may be a target of AMKL.

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