STMN1 (stathmin 1)

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Effect of the p53–tristetraprolin–stathmin-1 pathway on trophoblasts at maternal–fetal interface

PROBLEM To reveal the effect of p53-tristetraprolin-stathmin-1 signaling on trophoblasts and recurrent spontaneous abortion (RSA). METHOD OF STUDY Stathmin-1 (STMN1), p53, and tristetraprolin (TTP) expression in paraffin-embedded villus tissue was determined using immunohistochemistry. HTR-8/SVneo cells were treated with doxorubicin to activate p53; STMN1 and TTP levels were detected by quant...

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Stathmin 1 in normal and malignant hematopoiesis

Stathmin 1 is a microtubule destabilizer that plays an important role in cell cycle progression, segregation of chromosomes, clonogenicity, cell motility and survival. Stathmin 1 overexpression has been reported in malignant hematopoietic cells and Stathmin 1 inhibition reduces the highly proliferative potential of leukemia cell lines. However, during the differentiation of primary hematopoieti...

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Stathmin 1 expression in plasma cell neoplasms

Multiple myeloma (MM) is a hematological malignancy characterized by clonal proliferation of malignant plasma cells which accumulate in the bone marrow, resulting in recurrent hypercalcemia, anemia, osteolytic lesions, renal failure, and increased risk of infection.1 Stathmin 1, also named oncoprotein 18 (OP18) or leukemia-associated phosphoprotein p18 (LAP18), is a microtubule destabilizer tha...

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Unbiased proteomic and transcript analyses reveal that stathmin-1 silencing inhibits colorectal cancer metastasis and sensitizes to 5-fluorouracil treatment.

UNLABELLED Colorectal cancer metastasis is a major cause of mortality worldwide, which may only be controlled with novel methods limiting tumor dissemination and chemoresistance. High stathmin-1 (STMN1) expression was previously established as a hallmark of colorectal cancer progression and predictor of poor survival; however, the mechanism of action is less clear. This work demonstrates that S...

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Stathmin 1 inhibition amplifies ruxolitinib-induced apoptosis in JAK2V617F cells

The JAK/STAT pathway is constitutively activated in myeloproliferative neoplasms and can be inhibited by ruxolitinib, a selective JAK1/2 inhibitor. The JAK2(V617F) mutation leads to constitutive STAT3 phosphorylation and potentially leads to inhibition of Stathmin 1 activity via STAT3. In support of this hypothesis, we found that, in HEL JAK2(V617F) cells, ruxolitinib treatment decreased STAT3 ...

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ژورنال

عنوان ژورنال: Atlas of Genetics and Cytogenetics in Oncology and Haematology

سال: 2015

ISSN: 1768-3262

DOI: 10.4267/2042/56298