Cantharidin induces apoptosis of human multiple myeloma cells via inhibition of the JAK/STAT pathway
نویسندگان
چکیده
منابع مشابه
Matrine induces apoptosis of human multiple myeloma cells via activation of the mitochondrial pathway.
Multiple myeloma (MM) is a hematological malignancy characterized by the uncontrolled proliferation of clonal plasma cells in bone marrow in the elderly. Although there have been tremendous advances in the treatment of MM, it remains an incurable disease. Matrine, a main alkaloid of the traditional Chinese herb Sophora flavescens Ait, has been shown to inhibit cellular proliferation and induce ...
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Multiple Myeloma (MM) is an incurable hematological malignancy affecting millions of people worldwide. As in all tumor cells both glucose and more recently glutamine have been identified as important for MM cellular metabolism, however there is some dispute as to the role of glutamine in MM cell survival. Here we show that the small molecule inhibitor compound 968 effectively inhibits glutamina...
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Objective(s): The aim of this study was to determine the important molecules involved in apoptosis induction by opium in Jurkat cell line. Materials and Methods: Jurkat cells were incubated 48 hrs with2.86×10-5 g/ml concentration of opium and apoptosis as well as expression levels of related molecules weremeasured. Results: Our results demonstrated that 50.3±0.2 percent of opium treated Jurka...
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متن کامل2,5-Dihydroxyacetophenone Induces Apoptosis of Multiple Myeloma Cells by Regulating the MAPK Activation Pathway.
2,5-Dihydroxyacetophenone (DHAP) is an active compound obtained from Radix rehmanniae preparata, which is widely used as a herbal medicine in many Asian countries. DHAP has been found to possess anti-inflammatory, anti-anxiety, and neuroprotective qualities. For the present study, we evaluated the anti-cancer effects of DHAP on multiple myeloma cells. It was discovered that DHAP downregulated t...
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ژورنال
عنوان ژورنال: Cancer Science
سال: 2008
ISSN: 1347-9032,1349-7006
DOI: 10.1111/j.1349-7006.2008.00872.x