Reduction of Hematopoietic Cell-Specific Tyrosine Phosphatase SHP-1 Gene Expression in Natural Killer Cell Lymphoma and Various Types of Lymphomas/Leukemias

Oka, Takashi; Yoshino, Tadashi; Hayashi, Kazuhiko; Ohara, Nobuya; Nakanishi, Tohru; Yamaai, Yuichiro; Hiraki, Akio; Sogawa, Chiharu; Kondo, Eisaku; Teramoto, Norihiro; Takahashi, Kiyoshi; Tsuchiyama, Junjiro; Akagi, Tadaatsu

doi:10.1016/s0002-9440(10)62535-7

Cited by 100 publications

(102 citation statements)

References 48 publications

(41 reference statements)

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“…Our observation showing increased proliferation following inhibition of SHP1 by antisense oligonucleotides in MCF-7 cells is consistent with a role for SHP1 in the negative regulation of mitogenic pathways in hematopoietic cells (15,17,18). The loss or diminished expression of SHP1 observed in leukemias and lymphomas (33) suggest that SHP1 function plays a vital role in the suppression of undesired cell proliferation. In contrast to hematopoietic tumors, SHP1 mRNA was reported to be increased in estrogen receptor-positive and -negative breast cancer cell lines and in 58% of the primary breast tumors compared with normal breast cells (23).…”

Section: Discussionsupporting

confidence: 86%

Breast Cancer Cells Proliferation Is Regulated by Tyrosine Phosphatase SHP1 through c-jun N-Terminal Kinase and Cooperative Induction of RFX-1 and AP-4 Transcription Factors

Amin

Kumar

Nilchi

et al. 2011

Molecular Cancer Research

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In this study, we show that proliferation of breast cancer cells is suppressed by IGF-1-activated JNK MAPK pathway. The molecular mechanism by which c-jun-NH,-kinase (JNK) activation induces antiproliferative signals in IGF-1-stimulated breast cancer cells remains unknown. Tyrosine phosphatase SHP1 is known to negatively regulate signal transduction pathways activated by cell surface receptors including IGF-1. Moreover, SHP1 transcript and protein levels are increased in epithelial tumors. Therefore, we hypothesized that IGF-activated JNK induces expression of SHP1 in breast cancer cells. To further clarify the role of SHP1 in tumor growth, we correlated the proliferation rates of breast adenocarcinoma cells with SHP1 expression and JNK activation. We show that proliferation of serum-or IGF-1-stimulated breast adenocarcinoma cells is negatively regulated by SHP1 and show for the first time that IGF-1-activated JNK induces SHP1 expression in MCF-7 cells used as experimental model. In an attempt to understand the mechanism by which serum-or IGF-1-activated JNK induces SHP1 expression resulting in suppression of cell proliferation, we reveal for the first time that in serum-or IGF-1-stimulated breast cancer MCF-7 cells, JNK induces SHP1 expression through the binding of AP-4 and RFX-1 transcription factors to the epithelial tissue-specific SHP1 promoter. Overall, we show for the first time that IGF-1-stimulated proliferation of breast adenocarcinoma cells is negatively regulated by SHP1 through activation of JNK. Mol Cancer Res; 9(8); 1112-25. Ó2011 AACR.

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Section: Discussionsupporting

confidence: 86%

Breast Cancer Cells Proliferation Is Regulated by Tyrosine Phosphatase SHP1 through c-jun N-Terminal Kinase and Cooperative Induction of RFX-1 and AP-4 Transcription Factors

Amin

Kumar

Nilchi

et al. 2011

Molecular Cancer Research

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“…Only a few genome-wide profiling studies using NK-cell lines 13,14 and a limited number of NK-cell 15 and gd T-cell lymphoma cases have been performed. 16 In this study, we have defined molecular signatures for ENKTL and related malignancies.…”

Section: Introductionmentioning

confidence: 99%

Natural killer cell lymphoma shares strikingly similar molecular features with a group of non-hepatosplenic γδ T-cell lymphoma and is highly sensitive to a novel aurora kinase A inhibitor in vitro

et al. 2010

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Natural killer cell lymphoma shares strikingly similar molecular features with a group of non-hepatosplenic cd T-cell lymphoma and is highly sensitive to a novel aurora kinase A inhibitor in vitro Natural killer (NK) cell lymphomas/leukemias are rare neoplasms with an aggressive clinical behavior. The majority of the cases belong to extranodal NK/T-cell lymphoma, nasal type (ENKTL) in the current WHO classification scheme. Geneexpression profiling (GEP) of 21 ENKTL and NK-cell lymphoma/ leukemia patients, 17 NK-and T-cell lines and 5 indolent NK-cell large-granular-lymphocytic proliferation was performed and compared with 125 peripheral T-cell lymphoma (PTCL) patients previously studied. The molecular classifier derived for ENKTL patients was comprised of 84 transcripts with the majority of them contributed by the neoplastic NK cells. The classifier also identified a set of cd-PTCLs both in the ENKTL cases as well as in cases initially classified as PTCL-not otherwise specified. These cd-PTCLs expressed transcripts associated with the T-cell receptor (TCR)/CD3 complex, suggesting T cell rather than NK-cell lineage. They were very similar to NK-cell tumors by GEP, but were distinct from cytotoxic (ab)-PTCL and hepatosplenic T-cell lymphoma, indicating derivation from an ontogenically and functionally distinct subset of cd T cells. They showed distinct expression of Vc9, Vd2 transcripts and were positive for TCRc, but negative for TCRb by immunohistochemistry. Targeted inhibition of two oncogenic pathways (AURKA and NOTCH-1) by small-molecular inhibitors induced significant growth arrest in NK-cell lines, thus providing a rationale for clinical trials of these inhibitors in NK-cell malignancies.

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“…A large number of studies have been focused on the role of SHP-1 in hematopoietic cells, 13,[34][35][36][37] whereas the role of SHP-1 in epithelial cells and epithelium-derived carcinomas is less well characterized. In hematopoietic cells, SHP-1 has been suggested to contribute to the termination of mitogenic signals of growth factors by dephosphorylating critical phosphorylated molecules.…”

Section: Discussionmentioning

confidence: 99%

“…Decreased or abolished expression in leukemia and lymphoma has been related to both malignant transformation and tumor cell invasiveness. [12][13][14] Moreover, SHP-1 expression in leukemic cells can lead to decreased proliferation and induction of morphological changes. 15 Transient transfection of SHP-1 in the breast cancer cell line MDA-MB-231, with undetectable endogenous SHP-1, reduced cell proliferation 2-3 fold.…”

mentioning

confidence: 99%

Immunohistochemical detection of tyrosine phosphatase SHP‐1 predicts outcome after radical prostatectomy for localized prostate cancer

Tassidis

Brokken

Jirström

et al. 2010

Intl Journal of Cancer

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The protein tyrosine kinase (PTK) receptors and cytosolic signaling proteins as well as the protein tyrosine phosphatases (PTPs) have important roles in regulation of growth of the benign and malignant prostate gland. Here, we studied expression of the protein tyrosine phosphatase SHP-1 in prostate cancer cell lines and in human prostatic tissues. SHP-1 is expressed at a high level in LNCaP prostate cancer cells compared with PC3 cells. Silencing of SHP-1 expression with siRNA in LNCaP cells led to an increased rate of proliferation, whereas overexpression of SHP-1 by means of transient and stable transfection in PC3 cells led to a decrease in proliferation. Corresponding changes were observed in cyclin D1 expression. We further demonstrate that LNCaP and PC3 cells respond differently to IL-6 stimulation. SHP-1 overexpression in PC3 cells reversed IL-6 stimulation of proliferation, whereas in SHP-1-silenced LNCaP cells, IL-6 inhibition of proliferation was not affected. In addition, IL-6 treatment led to higher levels of phosphorylated STAT3 in SHP-1-silenced LNCaP cells than in control cells. Next, SHP-1 expression in human prostate cancer was analyzed by immunohistochemical staining of tissue microarrays comprising tumor specimens from 100 prostate cancer patients. We found an inverse correlation between the tumor level of SHP-1 expression and time to biochemical recurrence and clinical progression among prostate cancer patients. In conclusion, our results suggest that a decreased level of SHP-1 expression in prostate cancer cells is associated with a high proliferation rate and an increased risk of recurrence or clinical progression after radical prostatectomy for localized prostate cancer.

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Reduction of Hematopoietic Cell-Specific Tyrosine Phosphatase SHP-1 Gene Expression in Natural Killer Cell Lymphoma and Various Types of Lymphomas/Leukemias

Cited by 100 publications

References 48 publications

Breast Cancer Cells Proliferation Is Regulated by Tyrosine Phosphatase SHP1 through c-jun N-Terminal Kinase and Cooperative Induction of RFX-1 and AP-4 Transcription Factors

Breast Cancer Cells Proliferation Is Regulated by Tyrosine Phosphatase SHP1 through c-jun N-Terminal Kinase and Cooperative Induction of RFX-1 and AP-4 Transcription Factors

Natural killer cell lymphoma shares strikingly similar molecular features with a group of non-hepatosplenic γδ T-cell lymphoma and is highly sensitive to a novel aurora kinase A inhibitor in vitro

Immunohistochemical detection of tyrosine phosphatase SHP‐1 predicts outcome after radical prostatectomy for localized prostate cancer

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