Positive interactions between STAP-1 and BCR-ABL influence chronic myeloid leukemia cell proliferation and survival

Ishiura, Marie; Kitai, Yuichi; Kashiwakura, Jun‐ichi; Muromoto, Ryuta; Toda, Jun; Ichii, Michiko; Oritani, Kenji; Matsuda, Tadashi

doi:10.1016/j.bbrc.2021.03.162

Cited by 7 publications

(2 citation statements)

References 25 publications

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“…[39] ABL1 can activate numerous pathways associated with growth promotion, cell survival, and disease progression. [40] The involvement of ABL1 in the development of CML has been widely investigated, for example, ABL1 overexpression promotes proliferative, invasive, and migratory behaviors of cells and EMT in CML via activating the PI3K/AKT/NF-κB pathway. [41,42] Despite that ABL1 was identified as a key regulator in PE, [43] the detailed function and the regulatory mechanism have never been explored before.…”

Section: Discussionmentioning

confidence: 99%

Hsa_circ_0088196 suppresses trophoblast migration and invasion by the miR‐525‐5p/ABL1 axis and the PI3K/AKT signaling pathway

Shi

2022

J Biochem & Molecular Tox

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Our study aimed to explore the role of circ_0088196 (circular TNC [circTNC]) in trophoblast invasion and migration in preeclampsia (PE) both in vitro and in vivo. CircTNC, miR‐525‐5p, and ABL1 expression in trophoblast HTR8/SVneo cells were evaluated by quantitative real‐time polymerase chain reaction (qRT‐PCR). Cell viability, migration, and invasion were detected by Cell Counting Kit‐8 (CCK‐8), wound healing, and Transwell assays. The binding between circTNC (or ABL1) and miR‐525‐5p was validated by RNA pulldown and luciferase reporter assays. The mouse model of PE was injected with sh‐circTNC and the effects of circTNC knockdown on the mean artery pressure, urine protein concentration, and fetal survival number of pregnant mice were examined. The expression of MMP‐2, MMP‐9, and PI3K/AKT pathway molecules in placental tissues was assessed by immunohistochemistry, qRT‐PCR, and western blot analysis. CircTNC overexpression inhibited cell invasion and migration, but did not influence cell proliferation. CircTNC bound with miR‐525‐5p, whose knockdown repressed cell invasion and migration, while it exerted no effect on cell proliferation. ABL1, a target of miR‐525‐5p, attenuated cell migration and invasion, without influence on cell viability. Importantly, either miR‐525‐5p overexpression or ABL1 depletion antagonized the repression of upregulated circTNC on trophoblast cell migration and invasion, MMP‐2 and MMP‐9 expression, and the PI3K/AKT pathway. CircTNC knockdown alleviated PE symptoms in pregnant mice. CircTNC knockdown promoted the trophoblast invasiveness in mice placenta by upregulating MMP‐2/9 expression and suppressing the PI3K/AKT pathway. Circ_0088196 represses trophoblast invasion and migration both in vitro and in vivo via regulating the miR‐525‐5p/ABL1 axis and activating the PI3K/AKT pathway.

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Section: Discussionmentioning

confidence: 99%

Hsa_circ_0088196 suppresses trophoblast migration and invasion by the miR‐525‐5p/ABL1 axis and the PI3K/AKT signaling pathway

Shi

2022

J Biochem & Molecular Tox

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“…We previously reported that STAP-1 is a key molecule that regulates chronic myeloid leukemia (CML) stem cell survival by increasing the anti-apoptotic gene expression via enhanced STAT5 activity. We also indicated a direct interaction between STAP-1, STAT5, and BCR–ABL in CML cells [ 25 , 26 ].…”

Section: Signal-transducing Adaptor Protein Family Of Proteinsmentioning

confidence: 99%

The Functional Properties and Physiological Roles of Signal-Transducing Adaptor Protein-2 in the Pathogenesis of Inflammatory and Immune Disorders

2022

Self Cite

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Adaptor molecules play a crucial role in signal transduction in immune cells. Several adaptor molecules, such as the linker for the activation of T cells (LAT) and SH2 domain-containing leukocyte protein of 76 kDa (SLP-76), are essential for T cell development and activation following T cell receptor (TCR) aggregation, suggesting that adaptor molecules are good therapeutic targets for T cell-mediated immune disorders, such as autoimmune diseases and allergies. Signal-transducing adaptor protein (STAP)-2 is a member of the STAP family of adaptor proteins. STAP-2 functions as a scaffold for various intracellular proteins, including BRK, signal transducer, and activator of transcription (STAT)3, STAT5, and myeloid differentiation primary response protein (MyD88). In T cells, STAP-2 is involved in stromal cell-derived factor (SDF)-1α-induced migration, integrin-dependent cell adhesion, and Fas-mediated apoptosis. We previously reported the critical function of STAP-2 in TCR-mediated T cell activation and T cell-mediated autoimmune diseases. Here, we review how STAP-2 affects the pathogenesis of T cell-mediated inflammation and immune diseases in order to develop novel STAP-2-targeting therapeutic strategies.

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Signal-transducing adaptor protein-1 and protein-2 in hematopoiesis and diseases

Ichii¹,

Oritani²,

Toda³

et al. 2022

Experimental Hematology

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Positive interactions between STAP-1 and BCR-ABL influence chronic myeloid leukemia cell proliferation and survival

Cited by 7 publications

References 25 publications

Hsa_circ_0088196 suppresses trophoblast migration and invasion by the miR‐525‐5p/ABL1 axis and the PI3K/AKT signaling pathway

Hsa_circ_0088196 suppresses trophoblast migration and invasion by the miR‐525‐5p/ABL1 axis and the PI3K/AKT signaling pathway

The Functional Properties and Physiological Roles of Signal-Transducing Adaptor Protein-2 in the Pathogenesis of Inflammatory and Immune Disorders

Signal-transducing adaptor protein-1 and protein-2 in hematopoiesis and diseases

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