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

Ikebuchi, Yuki; Ito, Kousei; Takada, Tappei; Anzai, Naohiko; Kanai, Yoshikatsu; Suzuki, Hiroshi

doi:10.1124/dmd.110.034603

Cited by 8 publications

(3 citation statements)

References 39 publications

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“…PDZK1 is reported to directly interact with multidrug resistance-associated protein (MRP) 2, which is expressed in small intestine and has at least partially overlapped substrate specificity with BCRP (Kocher et al, 1999), although there has been no evidence that small intestinal MRP2 is regulated by PDZK1. Post-transcriptional regulation of BCRP has recently been reported in various types of cells (Ikebuchi et al, 2010;Nagai et al, 2011;Sugiyama et al, 2011). Nevertheless, the present findings are the first evidence that PDZK1 is a functional regulator for BCRP in vivo in small intestine.…”

Section: Discussioncontrasting

confidence: 45%

PDZK1 Regulates Breast Cancer Resistance Protein in Small Intestine

Shimizu¹,

Sugiura²,

Wakayama³

et al. 2011

Drug Metab Dispos

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ABSTRACT:Transporter adaptor protein PDZK1 regulates several influx transporters for xenobiotics and nutrients in small intestine, and their expression on the apical membrane is diminished in pdzk1 gene knockout [pdzk1(؊/؊)] mice. In the present study, we initially attempted to use pdzk1(؊/؊) mice to functionally identify influx transporters responsible for intestinal absorption of cimetidine. Contrary to our expectation, the plasma concentration of cimetidine after oral administration to pdzk1(؊/؊) mice was higher than that in wild-type mice, and the double peaks of plasma concentration found in wild-type mice were not observed in pdzk1 (

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Section: Discussioncontrasting

confidence: 45%

PDZK1 Regulates Breast Cancer Resistance Protein in Small Intestine

Shimizu¹,

Sugiura²,

Wakayama³

et al. 2011

Drug Metab Dispos

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“…1999). RACK1 regulates the plasma membrane localization of some proteins [35,36]. RACK1 may play an essential role not only in activating Aurora-A for mitotic commitment, but also recruitment of the activators to centrosome.…”

Section: Discussionmentioning

confidence: 99%

RACK1 affects the progress of G2/M by regulating Aurora-A

Shen

Feng

et al. 2019

Cell Cycle

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Aurora-A is a serine/threonine kinase, which is overexpressed in multiple human cancers and plays a key role in tumorigenesis and tumor development. In this study, we found that the receptor of activated C-kinase1 (RACK1), an important regulator of biological functions, interacted with Aurora-A and co-localized with Aurora-A at centrosomes. Moreover, RACK1 induces the autophosphorylation of Aurora-A in vitro and in vivo. Depletion of RACK1 impaired the activation of Aurora-A in late G2 phase, then inhibited the mitotic entry and leaded to multi-polarity, severe chromosome alignment defects, or centrosome amplification. Taken together, these results suggest that RACK1 is a new partner of Aurora-A and play a critical role in the regulation of the Aurora-A activity during mitosis, which may provide a basis for future anticancer studies targeting Aurora-A.

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“… 14 It is confirmed that RACK1 can regulate several apoptosis-related genes and drug-related genes and then lead to the occurrence of chemotherapy resistance. 15 , 16 Furthermore, recent study showed that the expression level of RACK1 in tumor tissue was correlated with the chemoresistance of HCC. 12 In the current study, we aimed to evaluate the role of RACK1 in proliferation and its involvement in the underlying mechanism of chemotherapy resistance in ESCC.…”

Section: Introductionmentioning

confidence: 99%

RACK1 induces chemotherapy resistance in esophageal carcinoma by upregulating the PI3K/AKT pathway and Bcl-2 expression

Liu

Chen

Cheng

et al. 2018

OTT

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IntroductionAccumulating evidence indicates that RACK1 is involved in the progression of tumors. We aimed to evaluate the function of RACK1 in esophageal squamous cell carcinoma (ESCC) and its role in the mechanism of chemotherapy resistance.Materials and methodsTransfected ESCC cell lines with plasmids expressed shRACK1 or open reading frame (ORF) targeting RACK1 and established stable cell lines. We then examined the effects of RACK1 on cell proliferation and chemotherapy resistance in ESCC cell lines, and the expression of AKT, pAKT, ERK1/2, Bcl-2, and Bim was introduced to further detect the association between RACK1 and chemotherapy resistance.ResultsThe proliferation ability of ESCC cells was improved in the overexpression RACK1 groups (P<0.001) and decreased in the transfected shRACK1 groups (P<0.001) compared with the control ones. Meanwhile, upregulation of RACK1 significantly suppressed cisplatin-induced apoptosis in Eca109 and EC9706 cells, while downregulation of RACK1 promoted the sensitivity compared to the control group (Eca109: P<0.001 for shRACK1, P<0.01 for shNC, and P<0.001 for overexpression group; EC9706: P<0.001 for shRACK1, P<0.001 for shNC, and P<0.05 for overexpression group). Furthermore, we found that RACK1 could activate the PI3K/AKT pathway and increase the expression level of Bcl-2 in ESCC, which leads to the enhancement of chemoresistance in ESCC.ConclusionRACK1 promotes proliferation and chemotherapy resistance in ESCC by activating the PI3K/AKT pathway and upregulating the Bcl-2 expression.

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

Cited by 8 publications

References 39 publications

PDZK1 Regulates Breast Cancer Resistance Protein in Small Intestine

PDZK1 Regulates Breast Cancer Resistance Protein in Small Intestine

RACK1 affects the progress of G2/M by regulating Aurora-A

RACK1 induces chemotherapy resistance in esophageal carcinoma by upregulating the PI3K/AKT pathway and Bcl-2 expression

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