The essential roles of matrix metalloproteinase-2, membrane type 1 metalloproteinase and tissue inhibitor of metalloproteinase-2 in the invasive capacity of acute monocytic leukemia SHI-1 cells

Chen, Zixing; Li, Zhenjiang

doi:10.1016/j.leukres.2010.01.016

Cited by 31 publications

(30 citation statements)

References 29 publications

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“…Studies have confirmed that MMP-2 and MMP-9 play an important role in the invasion process of various solid tumors (Ray et al, 1994) and are also abnormally expressed in AML; their expression levels are correlated with extramedullary infiltration by leukemia cells (Reikvam et al, 2010). Feng reported that tight junction proteins were more obviously disrupted in SHI-1 cells than in the HL-60 and U937 leukemic cell lines, which is consistent with the higher rate of invasion of SHI-1 cells and the high constitutive expression of MMP-2 and MMP-9 in this cell line (Feng et al, 2011;Wang et al, 2010). MMP-2 and MMP-9 are tightly regulated at the levels of transcription and secretion by multiple factors.…”

Section: Discussionmentioning

confidence: 55%

Curcumin induces apoptosis and suppresses invasion through MAPK and MMP signaling in human monocytic leukemia SHI-1 cells

Zeng

Dai

Jiang

et al. 2015

Pharmaceutical Biology

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Curcumin inhibited SHI-1 cell proliferation by arresting the cells in the S-phase, increasing the number of Annexin V-FITC + /PI À cells and promoting the loss of 4W m . The results of PCR and Western blotting showed that curcumin increased the FasL mRNA level; inhibited Bcl-2, NF-jB, and ERK expression; and activated P38 MAPK, JNK, and caspase-3. Additionally, curcumin partially suppressed SHI-1 cell invasion and attenuated the mRNA transcription and secretion of MMP-2 and MMP-9. Discussion and conclusion: This study demonstrates that curcumin not only induces SHI-1 cell apoptosis, possibly via both intrinsic and extrinsic pathways triggered by JNK, P38 MAPK and ERK signaling, but also partially suppresses SHI-1 cell invasion, likely by reducing the levels of transcription and secretion of MMP-2 and MMP-9. KeywordsAntitumor, matrix metalloproteinase, mitogen-activated protein kinase History

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Section: Discussionmentioning

confidence: 55%

Curcumin induces apoptosis and suppresses invasion through MAPK and MMP signaling in human monocytic leukemia SHI-1 cells

Zeng

Dai

Jiang

et al. 2015

Pharmaceutical Biology

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“…Stefanidakis and colleagues suggested that EMD represents an ability of leukemic blasts to invade the surrounding tissues and showed that specific interaction between the matrix metalloproteinase (MMP)-9 and the leukocyte surface beta (2) integrin is required for the migration of AML-derived cells [Stefanidakis et al 2009]. Similarly, Wang and colleagues found a higher expression of MMP-2, membrane type 1 metalloproteinase and tissue inhibitor of metalloproteinase-2 in the highly invasive AML cell line SHI-1, coupled with a higher capacity for an in vitro invasion compared with other, noninvasive leukemic cell lines, supporting the role for MMPs in extramedullary blast penetration [Wang et al 2010].…”

Section: Pathogenesis Of Extramedullary Diseasementioning

confidence: 86%

Myeloid sarcoma: current approach and therapeutic options

Avni

Koren‐Michowitz

2011

Therapeutic Advances in Hematology

207

288

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Myeloid sarcoma is a rare disease that can present as an isolated extramedullary leukemic tumor, concurrently with or at relapse of acute myeloid leukemia. Owing to the rarity of this disorder, most of the literature comprises small retrospective studies and case reports. The aim of this review is to summarize the current published data regarding the clinical presentation, morphological, cytogenetic and molecular features, prognosis and treatment of myeloid sarcoma.

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“…For example, in SHI-1 cells, a highly invasive human acute monocytic leukemia cell line, there is a high expression level of matrix metalloproteinase 2 (MMP-2), membranetype 1 MMP and tissue inhibitor of metalloproteinase, which facilitate cell invasion. [40] Moreover, it has been suggested that the specific binding of MMP-9 via its procatalytic domain to leukocyte surface I domains of beta-2 integrins is essential for precellular proteolysis and migration of AML-derived cells [41] [ Table 1]. …”

Section: Genetic and Molecular Features Of Extramedullary Infiltratiomentioning

confidence: 99%

Molecular and cellular aspects of extramedullary manifestations of acute myeloid leukemia

Mohammadi-Asl¹,

Khosravi²,

Shahjahani³

et al. 2015

J Cancer Metastasis Treat

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The myeloid extramedullary tumor is a solid tumor formed by infiltration of immature myeloid cells in various tissues of the body. This tumor is also identified as chloroma or myeloid sarcoma (MS). MS is a manifestation of acute myeloid leukemia (AML) occurring at presentation or during treatment or relapse. MS is associated with multiple chromosomal abnormalities and molecular mutations since patients with these disorders bear a high potential for MS manifestation. There is a high incidence of extramedullary infiltration (EMI) in AML. AML patients with EMI have a worse prognosis than patients without it. Hematopoietic stem cells and leukemic stem cells reside in a special bone marrow microenvironment called niche, which is essential for their normal functions. Cancers are exploited dysfunctional cell-cell and matrix-cell interactions, which convert a normal niche into a neoplastic niche. This study summarizes the current knowledge on the molecular and cellular characteristics of AML with EMI and extramedullary niches in AML patients.

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The essential roles of matrix metalloproteinase-2, membrane type 1 metalloproteinase and tissue inhibitor of metalloproteinase-2 in the invasive capacity of acute monocytic leukemia SHI-1 cells

Cited by 31 publications

References 29 publications

Curcumin induces apoptosis and suppresses invasion through MAPK and MMP signaling in human monocytic leukemia SHI-1 cells

Curcumin induces apoptosis and suppresses invasion through MAPK and MMP signaling in human monocytic leukemia SHI-1 cells

Myeloid sarcoma: current approach and therapeutic options

Molecular and cellular aspects of extramedullary manifestations of acute myeloid leukemia

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