Roles of Stat3 and ERK in G‐CSF Signaling

Kamezaki, Kenjirou; Shimoda, Kazuya; Numata, Akihiko; Haro, Takashi; Kakumitsu, Haruko; Yoshie, Masumi; Yamamoto, Masahiro; Takeda, Kiyoshi; Matsuda, Tadashi; Akira, Shizuo; Ogawa, Katsuhiro; Harada, Mine

doi:10.1634/stemcells.2004-0173a

Cited by 60 publications

(67 citation statements)

References 49 publications

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“…In addition, signaling via other pathways, including those involving both PI 3-kinase and MEK, also appears to make a contribution to the enhanced mitogenic response. In contrast, STAT3 appears to exert a negative influence, in agreement with recent studies showing that STAT3 inhibits proliferative responses in the context of the full-length G-CSF-R. 40,41 Therefore, it is likely that the consequences of receptor truncation are a result of the net effect of a complex combination of signals, at least in 32D and gcsfr-D715/D715 cells, although it remains to be confirmed in primary cells from appropriate SCN/AML patients.…”

Section: Discussionsupporting

confidence: 87%

Multiple pathways contribute to the hyperproliferative responses from truncated granulocyte colony-stimulating factor receptors

et al. 2006

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Section: Discussionsupporting

confidence: 87%

Multiple pathways contribute to the hyperproliferative responses from truncated granulocyte colony-stimulating factor receptors

et al. 2006

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“…DUSP6 regulates ERK1/2, which is involved in the phosphorylation of many proteins including transcription factors, receptors and cytoskeletal proteins 3131, 32 as well as p‐AKT, which is a known target of L1 signaling, were studied. Both p‐AKT and p‐ERK levels were reduced following NFASC silencing, indicating that these signaling pathways might be of importance in understanding the effects of NFASC on NSCLC progression.…”

Section: Discussionmentioning

confidence: 99%

Copy number variation, increased gene expression, and molecular mechanisms of neurofascin in lung cancer

Erdem

Arnoldussen

Skaug

et al. 2017

Molecular Carcinogenesis

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Metastasis and cell adhesion are key aspects of cancer progression. Neurofascin (NFASC) is a member of the immunoglobulin superfamily of adhesion molecules and, while studies on NFASC are inadequate, other members have been indicated pivotal roles in cancer progression and metastasis. This study aimed at increasing the knowledge on the involvement of adhesion molecules in lung cancer progression by studying the regulation and role of NFASC in non‐small cell lung cancer (NSCLC). Here, copy number variations in the NFASC gene were analyzed in tumor and non‐tumorous lung tissues of 204 NSCLC patients. Frequent gene amplifications (OR = 4.50, 95%CI: 2.27‐8.92, P ≤ 0.001) and increased expression of NFASC (P = 0.034) were identified in tumors of NSCLC patients. Furthermore, molecular mechanisms of NFASC in lung cancer progression were evaluated by investigating the effects of NFASC silencing on cell proliferation, viability, migration, and invasion using siRNA technology in four NSCLC cell lines. Silencing of NFASC did not affect cell proliferation or viability but rather decreased NSCLC cell migration (P ≤ 0.001) and led to morphological changes, rearrangements in the actin cytoskeleton and changes in F‐actin networks in migrating NSCLC cell lines. This study is the first to report frequent copy number gain and increased expression of NFASC in NSCLC. Moreover, these data suggest that NFASC is a novel regulator of NSCLC cell motility and support a role of NFASC in the regulation of NSCLC progression.

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“…To elucidate the signal transduction pathways involved in such up-regulation, we pretreated the cells with various inhibitors of multiple G-CSF-activated signaling pathways, including the MEK/ERK and Jak-Stat pathways (24,25). Pretreatment of bone marrow cells with the MEK1/2 inhibitors, PD98059 (Fig.…”

Section: Stat3 But Not Other Stat Family Members Nor Erk Is Requirementioning

confidence: 99%

Induction of Bv8 Expression by Granulocyte Colony-stimulating Factor in CD11b+Gr1+ Cells

Qu¹,

Zhuang²,

Yu³

et al. 2012

Journal of Biological Chemistry

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Roles of Stat3 and ERK in G‐CSF Signaling

Cited by 60 publications

References 49 publications

Multiple pathways contribute to the hyperproliferative responses from truncated granulocyte colony-stimulating factor receptors

Multiple pathways contribute to the hyperproliferative responses from truncated granulocyte colony-stimulating factor receptors

Copy number variation, increased gene expression, and molecular mechanisms of neurofascin in lung cancer

Induction of Bv8 Expression by Granulocyte Colony-stimulating Factor in CD11b+Gr1+ Cells

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