Newly identified tumor-associated role of human Sharpin

Jung, Jin‐Young; Kim, Jin Man; Park, Byoungwoo; Cheon, Yeongmi; Lee, Bogman; Choo, Seung Ho; Koh, Sang Seok; Lee, Soojin

doi:10.1007/s11010-010-0413-x

Cited by 59 publications

(69 citation statements)

References 13 publications

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“…Upregulation of SHARPIN in HCC [22] was confirmed in a previous study by our group [25] , in which SHARPIN expression was shown to be positively correlated with larger hepatic tumors, a higher histological grade, and therefore HCC progression. In recently published work, we examined the role of SHARPIN in the malignant phenotype characteristic of HCC [25] .…”

Section: Sharpin: Newly Identified Mediator Of Hcc Invasion and Progrsupporting

confidence: 68%

“…SHARPIN was identified as a commonly upregulated gene in liver and ovarian cancer by cDNA microarray analysis, although the case-sample size in that study was not large enough to allow definite conclusions [22] . SHARPIN is also amplified and upregulated in invasive ductal breast cancers [23] .…”

Section: Sharpin: Newly Identified Mediator Of Hcc Invasion and Progrmentioning

confidence: 92%

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Emerging role of SHARPIN in hepatocellular carcinoma progression

Tanaka

Tateishi²,

Koike³

2017

Can Cell Microenviron

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Hepatocellular carcinoma (HCC) is one of the most common cancers worldwide and the leading cause of cancer-related death, especially in less economically developed regions. Despite recent progress in the diagnosis and therapy of HCC, the long-term survival rate of HCC patients is unacceptably low, in part due to the frequent development of vascular invasion or distant metastasis. The cellular functions of shank-associated RH domain-interacting protein (SHARPIN, also known as SIPL1) include the regulation of inflammation, apoptosis, immune signaling, and cell motility. SHARPIN is up-regulated in various types of cancers including HCC and has been implicated in the genesis and progression of malignant tumors, but its exact role in tumorigenesis is largely unknown. Here we present evidence supporting a role for SHARPIN in HCC invasion and progression. We also discuss the potential of SHARPIN and related genes as therapeutic targets for this currently incurable cancer.

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Section: Sharpin: Newly Identified Mediator Of Hcc Invasion and Progrsupporting

confidence: 68%

Section: Sharpin: Newly Identified Mediator Of Hcc Invasion and Progrmentioning

confidence: 92%

Emerging role of SHARPIN in hepatocellular carcinoma progression

Tanaka

Tateishi²,

Koike³

2017

Can Cell Microenviron

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“…The observation that suppression of NF-κB activation by NF-κB decoy oligonucleotide reduced the size of the metastatic nodules of LM8 cells in the lung is consistent with our results (7). It has been recently shown that the introduction of SHARPIN, a component of LUBAC, enhanced the anchorageindependent growth of CHO cells, although the amounts of the other components of LUBAC were not determined (42). Collectively, LUBAC-induced NF-κB activation might be involved not only in the attachment of LM8 cells to the lung, but also in the other aspects of metastasis after extravasation, such as invasion activity and/or anoikis resistance, in our experimental model.…”

Section: Discussionmentioning

confidence: 67%

Activation of nuclear factor-kappa B by linear ubiquitin chain assembly complex contributes to lung metastasis of osteosarcoma cells

Tomonaga

Hashimoto²,

Tokunaga³

et al. 2011

Int J Oncol

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Abstract. NF-κB is involved in the metastasis of malignant cells. We have shown that NF-κB activation is involved in the pulmonary metastasis of LM8 cells, a highly metastatic subclone of Dunn murine osteosarcoma cells. Recently, it was determined that a newly identified type of polyubiquitin chain, a linear polyubiquitin chain, which is specifically generated by the linear ubiquitin chain assembly complex (LUBAC), plays a critical role in NF-κB activation. Here, we have evaluated the roles of LUBAC-mediated NF-κB activation in the development of lung metastasis of osteosarcoma cells. All three components of LUBAC (HOIL-1L, HOIP and SHARPIN) were highly expressed in LM8 cells compared to Dunn cells. Attenuation of LUBAC expression by stable knockdown of HOIL-1L in LM8 cells significantly suppressed NF-κB activity, invasiveness in vitro and lung metastasis. Induction of intracellular adhesion molecule-1 (ICAM-1) expression by LUBAC is involved in cell retention in the lungs after an intravenous inoculation of tumor cells. Moreover, we found that knockdown of LUBAC decreased not only the number but also the size of the metastatic nodules of LM8 cells in the lungs. These results indicate that LUBAC-mediated NF-κB activation plays crucial roles in several steps involved in metastasis, including extravasation and growth of osteosarcoma cells in the lung, and that suppression of LUBAC-mediated linear polyubiquitination activity may be a new approach to treat this life-threatening disease of young adolescents.

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“…SHARPIN gene encodes for phosphoproteins that are conserved mainly in the cytoplasm (Lim et al, 2001). Up-regulation of this gene in multiple human cancer types have been addressed for tumour-associated role in carcinogenesis (Jung et al, 2010). However, this gene has been identified to regulate intrinsic caspasedependent mitochondria pathway leading to keratinocyte apoptosis (Liang and Sundberg, 2011).…”

Section: Discussionmentioning

confidence: 99%

Expression Profile of Genes Modulated by Aloe emodin in Human U87 Glioblastoma Cells

Haris

Ismail²,

Idris³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Glioblastoma, the most aggressive and malignant form of glioma, appears to be resistant to various chemotherapeutic agents. Hence, approaches have been intensively investigated to targeti specific molecular pathways involved in glioblastoma development and progression. Aloe emodin is believed to modulate the expression of several genes in cancer cells. We aimed to understand the molecular mechanisms underlying the therapeutic effect of Aloe emodin on gene expression profiles in the human U87 glioblastoma cell line utilizing microarray technology. The gene expression analysis revealed that a total of 8,226 gene alterations out of 28,869 genes were detected after treatment with 58.6 µg/ml for 24 hours. Out of this total, 34 genes demonstrated statistically significant change (p<0.05) ranging from 1.07 to 1.87 fold. The results revealed that 22 genes were up-regulated and 12 genes were down-regulated in response to Aloe emodin treatment. These genes were then grouped into several clusters based on their biological functions, revealing induction of expression of genes involved in apoptosis (programmed cell death) and tissue remodelling in U87 cells (p<0.01). Several genes with significant changes of the expression level e.g. SHARPIN, BCAP31, FIS1, RAC1 and TGM2 from the apoptotic cluster were confirmed by quantitative real-time PCR (qRT-PCR). These results could serve as guidance for further studies in order to discover molecular targets for the cancer therapy based on Aloe emodin treatment.

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Newly identified tumor-associated role of human Sharpin

Cited by 59 publications

References 13 publications

Emerging role of SHARPIN in hepatocellular carcinoma progression

Emerging role of SHARPIN in hepatocellular carcinoma progression

Activation of nuclear factor-kappa B by linear ubiquitin chain assembly complex contributes to lung metastasis of osteosarcoma cells

Expression Profile of Genes Modulated by Aloe emodin in Human U87 Glioblastoma Cells

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