Acute promyelocytic leukemia

Tallman, Martin S.

doi:10.1016/j.beha.2014.04.010

Cited by 2 publications

(2 citation statements)

References 608 publications

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“…Leukemia is a malignant hematologic neoplasm that occurs at the level of hematopoietic stem cells, accounts for ~5% of all malignancies, and is one of the most common types of cancer among children and adolescents ( 1 ). Acute promyelocytic leukemia (APL), a high mortality-associated subtype of acute leukemia, predominantly manifests as disseminated intravascular coagulation or hyperfibrinolysis-induced severe bleeding ( 2 ). Chemotherapy with all-trans retinoic acid, anthracycline antibiotics and arsenic trioxide is a typical treatment for leukemia, and has been widely used with satisfactory effect ( 3 ).…”

Section: Introductionmentioning

confidence: 99%

Sorafenib inhibited cell growth through the MEK/ERK signaling pathway in acute promyelocytic leukemia cells

Zhang

Liu

et al. 2018

Oncol Lett

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The present study assessed the mechanism underlying the effect of sorafenib on the proliferation and apoptosis of the acute promyelocytic leukemia (APL) cell line NB4. NB4 cells were treated with different concentrations of sorafenib (0, 1.5, 3, 6, and 12 µM) for 24, 48 and 72 h. Cell proliferation, cell cycle, and apoptosis were analyzed using an MTT assay and flow cytometry analysis, respectively. Reverse transcription-semi-quantitative polymerase chain reaction and western blot analysis were performed to assess the expression of caspase-3, caspase-8, myeloid cell leukemia (MCL)1, cyclin D1, mitogen-activated protein kinase (MEK), phosphorylated (P)-MEK, extracellular signal-regulated kinase (ERK) and P-ERK. The results of the MTT assay demonstrated that, compared with untreated cells, the proliferation of sorafenib-treated NB4 cells was inhibited dose- and time-dependently. Furthermore, cell cycle arrest was induced in the G0/G1 phase and cell apoptosis was promoted in a dose-dependent manner in sorafenib-treated NB4 cells compared with untreated cells. In addition, the expression of the proapoptotic molecules caspase-3 and caspase-8 was significantly upregulated, and the expression of the antiapoptotic molecule MCL1 and the cell cycle-associated cyclin D1 was downregulated in sorafenib-treated NB4 cells compared with untreated cells. Furthermore, the phosphorylation of MEK and ERK was inhibited in sorafenib-treated NB4 cells compared with untreated cells. Sorafenib may inhibit proliferation and induce cell cycle arrest and apoptosis in APL cells. The underlying mechanisms of such effects may be associated with alterations to the expression of apoptosis-associated and cell cycle-associated molecules via MEK/ERK signaling pathway inhibition.

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Section: Introductionmentioning

confidence: 99%

Sorafenib inhibited cell growth through the MEK/ERK signaling pathway in acute promyelocytic leukemia cells

Zhang

Liu

et al. 2018

Oncol Lett

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“…A typical example is the effective applications of all-trans retinoic acid (ATRA, a vitamin A derivative) and arsenic trioxide (an ancient drug used in traditional Chinese medicine) in acute promyelocytic leukemia (APL, a subtype of acute myeloid leukemia (AML)), majority of which carry a chromosome translocation t (15;17) expressing the oncogenic promyelocytic leukemia retinoic acid receptor-alpha (PML-RAR) fusion protein [17]. Both drugs cleave or degrade the fusion protein, where arsenic trioxide was shown to bind directly to cysteine residues in zinc fingers located within the RBCC domain of PML-RAR and PML, inducing PML oligomerization and thus enhancing sumoylation and degradation of these two proteins [18].…”

mentioning

confidence: 99%

Natural products against hematological malignancies and identification of their targets

Xü

Liu

et al. 2015

Sci. China Life Sci.

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Acute promyelocytic leukemia

Cited by 2 publications

References 608 publications

Sorafenib inhibited cell growth through the MEK/ERK signaling pathway in acute promyelocytic leukemia cells

Sorafenib inhibited cell growth through the MEK/ERK signaling pathway in acute promyelocytic leukemia cells

Natural products against hematological malignancies and identification of their targets

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