Expression of RACK1 is a novel biomarker in pulmonary adenocarcinomas

Nagashio, Ryo; Sato, Yuichi; Matsumoto, Toshihide; Kageyama, Taihei; Satoh, Yukitoshi; Ryuge, Shinichiro; Masuda, Noriyuki; Goshima, Naoki; Jiang, Shi‐Xu; Okayasu, Isao

doi:10.1016/j.lungcan.2009.09.015

Cited by 63 publications

(61 citation statements)

References 26 publications

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“…It has been well established that ABCG2 excretes a wide range of anticancer drugs and its expression is significantly associated with response and progression-free survival in patients with small cell lung cancer treated with platinum-based chemotherapy (Kim et al, 2009). In addition, it has been recently shown that elevated RACK1 expression is not only closely related to in vitro cell proliferation and invasion (Berns et al, 2000) but also linked to in vivo growth and metastasis of pulmonary adenocarcinomas and breast carcinomas (Cao et al, 2010;Nagashio et al, 2010). From these observations, it is possible that RACK1 can be attributed to tumor genesis and the multidrug resistance phenotype through the positive regulation of ABCG2.…”

Section: Discussionmentioning

confidence: 99%

Receptor for Activated C-Kinase 1 Regulates the Cell Surface Expression and Function of ATP Binding Cassette G2

Ikebuchi¹,

Ito²,

Takada³

et al. 2010

Drug Metab Dispos

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ABSTRACT:In a previous report, we identified the receptor for activated Ckinase 1 (RACK1) as a positive regulator of the cellular localization and expression of ATP-binding cassette B4, a phosphatidylcholine translocator expressed on the bile canalicular membrane. In the present study, we focused on the role of RACK1 on ATP-binding cassette G2 (ABCG2), which is responsible for the cellular extrusion of compounds including antitumor drugs. Protein expression of ABCG2 was up-regulated by RACK1 overexpression, although mRNA expression of ABCG2 was not dependent on RACK1. The effect of RACK1 on the expression of ABCG2 on the cell surface was confirmed by the uptake of

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Section: Discussionmentioning

confidence: 99%

Receptor for Activated C-Kinase 1 Regulates the Cell Surface Expression and Function of ATP Binding Cassette G2

Ikebuchi¹,

Ito²,

Takada³

et al. 2010

Drug Metab Dispos

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“…Rack1 is highly expressed in many cancers, including pulmonary adenocarcinoma (Nagashio et al, 2009), colon carcinoma (Berns et al, 2000), melanoma (Egidy et al, 2008) and breast carcinoma (Cao et al, 2009a, b). In order to elucidate the role of Rack1 in tumorigenesis, the JB6 C141 (promotion sensitive, P þ ) mouse skin epidermal cell line (Bernstein and Colburn, 1989) was used.…”

Section: Rack1 Promotes Cell Transformation By Maintaining C-jun Protmentioning

confidence: 99%

“…Rack1 also promotes degradation of HIF1a (Liu et al, 2007) and BimEL (Zhang et al, 2008) by mediating the interaction between each of these proteins and the ubiquitin complex. Importantly, accumulating clinical data indicate that Rack1 is involved in cancer cell proliferation, invasion and metastasis, and is a novel biomarker for diagnosis and prognosis prediction (Wang et al, 2008;Nagashio et al, 2009;Cao et al, 2009aCao et al, , 2009b. These types of findings suggest that more studies are needed to increase our understanding as to how Rack1 functions in carcinogenesis.…”

Section: Introductionmentioning

confidence: 99%

Rack1 protects N-terminal phosphorylated c-Jun from Fbw7-mediated degradation

Zhang

Zhu

et al. 2011

Oncogene

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“…Recent studies have shown that RACK1 is a component of the 40S subunit of ribosome and present in both ribosome-and nonribosome-bound form (22)(23)(24). RACK1 is found to be upregulated in several kinds of tumors and considered as an excellent marker of oral squamous carcinoma, breast cancer, and pulmonary adenocarcinomas (25)(26)(27)(28)(29). Herein, we demonstrate that RACK1 is highly expressed in normal liver and frequently upregulated in HCC and that the ribosome localization is essential for RACK1-mediated in vitro chemoresistance and in vivo growth of HCC.…”

Section: Introductionmentioning

confidence: 99%

Ribosomal RACK1 promotes chemoresistance and growth in human hepatocellular carcinoma

Ruan¹,

Sun²,

Hao³

et al. 2012

J. Clin. Invest.

119

118

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Coordinated translation initiation is coupled with cell cycle progression and cell growth, whereas excessive ribosome biogenesis and translation initiation often lead to tumor transformation and survival. Hepatocellular carcinoma (HCC) is among the most common and aggressive cancers worldwide and generally displays inherently high resistance to chemotherapeutic drugs. We found that RACK1, the receptor for activated C-kinase 1, was highly expressed in normal liver and frequently upregulated in HCC. Aberrant expression of RACK1 contributed to in vitro chemoresistance as well as in vivo tumor growth of HCC. These effects depended on ribosome localization of RACK1. Ribosomal RACK1 coupled with PKCβII to promote the phosphorylation of eukaryotic initiation factor 4E (eIF4E), which led to preferential translation of the potent factors involved in growth and survival. Inhibition of PKCβII or depletion of eIF4E abolished RACK1-mediated chemotherapy resistance of HCC in vitro. Our results imply that RACK1 may function as an internal factor involved in the growth and survival of HCC and suggest that targeting RACK1 may be an efficacious strategy for HCC treatment.

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Expression of RACK1 is a novel biomarker in pulmonary adenocarcinomas

Cited by 63 publications

References 26 publications

Receptor for Activated C-Kinase 1 Regulates the Cell Surface Expression and Function of ATP Binding Cassette G2

Receptor for Activated C-Kinase 1 Regulates the Cell Surface Expression and Function of ATP Binding Cassette G2

Rack1 protects N-terminal phosphorylated c-Jun from Fbw7-mediated degradation

Ribosomal RACK1 promotes chemoresistance and growth in human hepatocellular carcinoma

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