Ser727/Tyr701-phosphorylated Stat1 is required for the regulation of c-Myc, cyclins, and p27Kip1 associated with ATRA-induced G0/G1 arrest of U-937 cells

Dimberg, Anna; Karlberg, Inger; Nilsson, Kenneth; Öberg, Fredrik

doi:10.1182/blood-2002-10-3149

Cited by 62 publications

(49 citation statements)

References 41 publications

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“…Once being phosphorylated, STAT1 molecules tend to form homodimers or heterotrimers with STAT2 and IFN regulatory factor 9 (IRF9), which, in turn, enable the complexes to translocate into the nucleus to enhance the transcription of numerous IFN stimulatory genes (ISGs) by binding to the specific elements, such as the IFN-stimulated response element (ISRE) or IFN-γ activated site (GAS) on their promoters (4). Worthy of mentioning, in line with the well-documented intensive cross-talk between IFN and RA signaling (5), all-trans retinoic acid (ATRA)-induced cell cycle arrest and differentiation of acute myeloid leukemia (AML) cells also involve the activation of STAT1 (6)(7)(8). As the direct target genes of STAT1 transcriptional activity, ISGs constitute the major effector molecules both in antiviral innate immunity by restricting viral RNA propagation (9,10) and in cellular proliferation regulation by inducing cell death and cell cycle arrest (11,12).…”

Section: Fns Consist Of Mainly Two Classes Of Related Cytokines Tymentioning

confidence: 99%

“…Previous studies demonstrate that the key IFN intracellular signaling mediator Stat1 acts as an oncorepressor in numerous tumor types (4). Relevant to this, it has been shown that analogous to the essential role of STAT1 activation in IFN intracellular signaling, the up-regulation and phosphorylation of STAT1 mediate the ATRA signaling-induced differentiation and growth inhibition of U937 cells (6,7), probably via promoting the expression of IFN and/or the numerous intracellular IFN signaling components (22,23). We then asked whether a functional relationship exists between RIG-I induction and STAT1 activation.…”

Section: Rig-i Induction Functionally Contributes To Ifn Plus Atra-inmentioning

confidence: 99%

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RA-inducible gene-I induction augments STAT1 activation to inhibit leukemia cell proliferation

Jiang

Zhang

Ding

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

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RA-inducible gene I (RIG-I/DDX58) has been shown to activate IFN-β promoter stimulator 1 (IPS-1) on recognizing cytoplasmic viral RNAs. It is unclear how RIG-I functions within the IFN and/or RA signaling process in acute myeloid leukemia (AML) cells, however, where obvious RIG-I induction is observed. Here, we show that the RIG-I induction functionally contributes to IFN-α plus RA-triggered growth inhibition of AML cells. Interestingly, although RIG-I induction itself is under the regulation of STAT1, a major IFN intracellular signal mediator, under circumstances in which it does not stimulate IPS-1, it conversely augments STAT1 activation to induce IFN-stimulatory gene expression and inhibit leukemia cell proliferation. Thus, our results unveil a previously undescribed RIG-I activity in regulating the cellular proliferation of leukemia cells via STAT1, which is independent of its classic role of sensing viral invasion to trigger type I IFN transcription.

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Section: Fns Consist Of Mainly Two Classes Of Related Cytokines Tymentioning

confidence: 99%

Section: Rig-i Induction Functionally Contributes To Ifn Plus Atra-inmentioning

confidence: 99%

RA-inducible gene-I induction augments STAT1 activation to inhibit leukemia cell proliferation

Jiang

Zhang

Ding

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

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“…STAT1 may contribute to ATRA-induced cell cycle arrest via regulation of cyclins, p27 Kip1 and c-Myc. 61,62 …”

Section: Jak-stat Pathwaymentioning

confidence: 99%

Signal transduction pathways that contribute to myeloid differentiation

Miranda

Johnson

2007

Leukemia

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The production of mature, differentiated myeloid cells is regulated by the action of hematopoietic cytokines on progenitor cells in the bone marrow. Cytokines drive the process of myeloid differentiation by binding to specific cell-surface receptors in a stage-and lineage-specific manner. Following the binding of a cytokine to its cognate receptor, intracellular signal-transduction pathways become activated that facilitate the myeloid differentiation process. These intracellular signaling pathways may promote myelopoiesis by stimulating expansion of a progenitor pool, supporting cellular survival during the differentiation process, or by directly driving the phenotypic changes associated with differentiation. Ultimately, pathways that drive the differentiation process converge on myeloid transcription factors, including PU.1 and the C/EBP family, that are critical for differentiation to proceed. While much is known about the cytokines, cytokine receptors and transcription factors that regulate myeloid differentiation, less is known about the precise roles that specific signaling mediators play in promoting myeloid differentiation. Recently, however, the application of novel pharmacologic inhibitors, siRNA strategies, and transgenic and knockout models has begun to shed light on the involvement and function of signaling pathways in normal myeloid differentiation. This review will discuss the roles that key signaling pathways and mediators play in myeloid differentiation.

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“…These findings contradict recent reports of a direct correlation among cyclin D1, c-Myc and Stat3 (28), but the downregulation of c-Myc by activation of Stat3 in tumor tissues has also been reported by other researchers (29), and cyclin D1 potentially creates a negative feedback loop onto Stat3 (30). in addition, Stat1 has been demonstrated to suppress c-Myc and cyclin D1 expression as a negative transcriptional regulator which relates to cell cycle arrest and an increase of P-Stat1 was observed in tKi-exposed cells in our experiments (31)(32)(33). Previous investigations have reported that Stat3 could lead to eMt, which may be helpful for chemoresistance (34-36), eMt was observed in tKi-exposed cells.…”

Section: Discussionmentioning

confidence: 91%

Continuous exposure of non-small cell lung cancer cells with wild-type EGFR to an inhibitor of EGFR tyrosine kinase induces chemoresistance by activating STAT3

Tang

Guo

et al. 2015

International Journal of Oncology

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Abstract. epidermal growth factor receptor-tyrosine kinase inhibitors (egfr-tKis) have shown promising effects against the growth of non-small cell lung cancer (nSclc) cells harboring egfr mutations (egfr-mts). However, many patients with nSclc that are accepted for egfr-tKi treatment followed by chemotherapy possess an unknown egfr status including wild-type egfr (egfr-wt). little is known about the potential effects of egfr-tKi treatment prior to chemotherapy. We investigated the effects and underlying molecular events of 4 weeks of continuous exposure to egfr-tKis in the egfr-wt nSclc line H1299. this treatment dramatically increased the ic 50 of several relevant chemotherapeutic agents: cisplatin (DDP) (29.25±6

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Ser727/Tyr701-phosphorylated Stat1 is required for the regulation of c-Myc, cyclins, and p27Kip1 associated with ATRA-induced G0/G1 arrest of U-937 cells

Cited by 62 publications

References 41 publications

RA-inducible gene-I induction augments STAT1 activation to inhibit leukemia cell proliferation

RA-inducible gene-I induction augments STAT1 activation to inhibit leukemia cell proliferation

Signal transduction pathways that contribute to myeloid differentiation

Continuous exposure of non-small cell lung cancer cells with wild-type EGFR to an inhibitor of EGFR tyrosine kinase induces chemoresistance by activating STAT3

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