RACK1 promotes hepatocellular carcinoma cell survival via CBR1 by suppressing TNF-α-induced ROS generation

Zhou, Silei; Cao, Huanling; Zhao, Yawei; Li, Xinying; Zhang, Jiyan; Hou, Chunmei; Ma, Yuanfang; Wang, Qingyang

doi:10.3892/ol.2016.5339

Cited by 13 publications

(7 citation statements)

References 23 publications

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“…Recently, studies indicated that RACK1 plays a dramatic role in the occurrence, development, and metastasis of various cancers, including non-small-cell lung cancer [ 15 – 17 ], hepatocellular carcinoma [ 18 , 19 ], esophageal squamous cell carcinoma [ 20 , 21 ], breast cancer [ 22 , 23 ], and prostate cancer [ 24 , 25 ]. However, reports about the function of RACK1 in cancer are inconsistent.…”

Section: Discussionmentioning

confidence: 99%

RACK1 Acts as a Potential Tumor Promoter in Colorectal Cancer

et al. 2019

Gastroenterology Research and Practice

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Background. The receptor of activated protein kinase C 1 (RACK1) promotes the progression and invasion of several cancers. However, the role of RACK1 in the pathogenesis of colorectal cancer (CRC) has not been clearly defined. Herein, we aimed to investigate the biological role of RACK1 in CRC. Materials and Methods. The Cancer Genome Atlas (TCGA) and the Gene Expression Omnibus (GEO) dataset were searched, and the expression of RACK1 in CRC tissues and adjacent normal tissues was evaluated. Immunohistochemical staining was performed to detect the expression of RACK1 in human CRC, adenoma, and normal tissues. Western blotting was used to detect the expression of RACK1 in human CRC cell lines. Functional assays, such as BrdU, colony formation, and wound healing and transwell invasion assays, were used to explore the biological role of RACK1 in CRC. Results. RACK1 was upregulated in CRC tissues compared with its expression in adjacent normal tissues in TCGA and the GEO dataset (P<0.05). Moreover, RACK1 was significantly overexpressed in CRC and adenoma tissues compared with its expression in normal tissues (P<0.05). Loss-of-function experiments showed that RACK1 promoted cell proliferation, migration, and invasion in vitro. Conclusions. Our data indicated that RACK1, as an oncogene, markedly promoted the progression of CRC, which suggested that RACK1 is a potential therapeutic target for CRC management.

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Section: Discussionmentioning

confidence: 99%

RACK1 Acts as a Potential Tumor Promoter in Colorectal Cancer

et al. 2019

Gastroenterology Research and Practice

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“…On the one hand, Chen et al11 found that loss of RACK1 enhanced gastric cancer metastasis. Additionally, Deng et al proved that RACK1 suppressed gastric tumorigenesis 12. On the other hand, there were other kinds of research which demonstrated that RACK1 was found to promote lung cancer cell growth 13.…”

Section: Discussionmentioning

confidence: 99%

<p>Downregulated expression of RACK1 results in pancreatic cancer growth and metastasis</p>

Zhang

Rong

et al. 2019

OTT

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BackgroundThe expression and function of the Receptor for Activated C Kinase 1 (RACK1) in cancer growth and metastasis are confused in different cancers, especially in pancreatic ductal adenocarcinoma (PDAC).MethodsOne-hundred and eighty-two PDAC tissue specimens (95 males and 87 females) including pancreatic cancer tissue and para-carcinoma tissue were collected for analysis between 2005 to 2012. Blood phenotypic parameters using cell count and capillary electrophoresis were investigated. HE staining, real time PCR, Western blot analysis, and soft agar assays were performed to determine the role of RACK1.PurposeIn this study, we aim to determine the specific role of RACK1 in the untility of PDAC.ResultsWe found that RACK1 expression was significantly lower in pancreatic cancer tissue than in para-carcinoma normal pancreatic tissue both in clinic and mice with pancreatic cancer at the early stage. Our results suggested that RACK1 silence could significantly promote cell growth and metastasis of pancreatic cancer cells. But we found that the overexpression of RACK1 has the opposite effect in vitro. In vivo MIAPaca-2 cells overexpressing RACK1, the results demonstrated lower metastatic ability than MIAPaca-2 cells. RACK1 overexpression could decrease the NF-κB transactivation activity of MIAPaca-2 cells, which was consistent with the inhibitory effect of RACK1 overexpression on the pro-migration and pro-invasive target gene of NF-κB, while which could be increased by RACK1 silence. RACK1 silence also enhanced protein expression of pro-migration and pro-invasive NF-κB target genes, which on the contrary, could be reversed by IκBα. Besides, RACK1 expression was significantly associated with lymph node metastasis, vessels metastasis, invasion of nerves as well as TNM staging. The 3-year survival rate of patients with high RACK1 expression was significantly higher than those patients with low RACK1 expression. However, RACK1 expression was not an independent risk factor for of the long-term postoperative survival of patients with pancreatic cancer.ConclusionThe obtained results in our study suggested that the low expression of RACK1 was associated with cancer cell growth and metastasis in pancreatic cancer through the activation of the NF-κB pathway. RACK1 could be a potential therapeutic drug target to pancreatic cancer and metastasis.

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“…RACK1 is a small promiscuous scaffolding protein that interacts with many receptors and signaling molecules (Adams, Ron, & Kiely, 2011; Erbil et al, 2016; Zhao et al, 2015; Zhou et al, 2016). For example, in dopamine neurons, RACK1 binds to dopamine transporter (DAT) and regulates the DAT phosphorylation by protein kinase C (PKC) (Lee, Kim, Kim, & Lee, 2004).…”

Section: Nhe9 Cellular Functionsmentioning

confidence: 99%

Sodium hydrogen exchanger 9 NHE9 (SLC9A9) and its emerging roles in neuropsychiatric comorbidity

Patak

Faraone

Zhang‐James

2020

American J of Med Genetics Pt B

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Variations in SLC9A9 gene expression and protein function are associated with multiple human diseases, which range from Attention-deficit/hyperactivity disorder (ADHD) to glioblastoma multiforme. In an effort to determine the full spectrum of human disease associations with SLC9A9, we performed a systematic review of the literature. We also review SLC9A9's biochemistry, protein structure, and function, as well as its interacting partners with the goal of identifying mechanisms of disease and druggable targets. We report gaps in the literature regarding the genes function along with consistent trends in disease associations that can be used to further research into treating the respective diseases. We report that SLC9A9 has strong associations with neuropsychiatric diseases and various cancers. Interestingly, we find strong overlap in SLC9A9 disease associations and propose a novel role for SLC9A9 in neuropsychiatric comorbidity. In conclusion, SLC9A9 is a multifunctional protein that, through both its endosome regulatory function and its protein-protein interaction network, has the ability to modulate signaling axes, such as the PI3K pathway, among others.

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RACK1 promotes hepatocellular carcinoma cell survival via CBR1 by suppressing TNF-α-induced ROS generation

Cited by 13 publications

References 23 publications

RACK1 Acts as a Potential Tumor Promoter in Colorectal Cancer

RACK1 Acts as a Potential Tumor Promoter in Colorectal Cancer

<p>Downregulated expression of RACK1 results in pancreatic cancer growth and metastasis</p>

Sodium hydrogen exchanger 9 NHE9 (SLC9A9) and its emerging roles in neuropsychiatric comorbidity

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