Silencing of CKIP-1 promotes tumor proliferation and cell adhesion-mediated drug resistance via regulating AKT activity in non-Hodgkins lymphoma

Zhu, Xinhua; Ouyang, Yu; Zhong, Fei; Wang, Qiru; Ding, Linlin; Zhang, Peipei; Liu, Hong; He, Song

doi:10.3892/or.2016.5233

Cited by 17 publications

(12 citation statements)

References 30 publications

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“…CKIP-1 also serves a role in numerous types of cancer, including colon and breast cancers, and human osteosarcoma. Knockdown of CKIP-1 promotes proliferation of NHL cells by altering the interaction with RAC-alpha serine/threonine-protein kinase (Akt) (27). CKIP-1 inhibits macrophage proliferation through activation of Akt (28).…”

Section: Discussionmentioning

confidence: 99%

miR‑98‑5p promotes osteoblast differentiation in MC3T3‑E1 cells by targeting CKIP‑1

et al. 2018

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Casein kinase 2-interacting protein 1 (CKIP-1) is a negative regulator for bone formation. Previously, using bioinformatics analysis, CKIP‑1 has been predicted to serve the role of target gene of miR‑98‑5p. In the present study, the potential role of miR‑98‑5p in regulating osteoblast differentiation through CKIP‑1 was investigated. Following pre‑treatment with microRNA (miR)‑98‑5p agomir or miR‑98‑5p antagomir, MC3T3‑E1 cells were cultured in an osteoinductive medium. Subsequently, the expression of miR‑98‑5p, CKIP‑1 and levels of osteoblast differentiation markers, including alkaline phosphatase, matrix mineralization, osteocaicin, collagen type I, runt‑related transcription factor 2 and osteopontin were assayed. Using a dual‑luciferase reporter assay, it was demonstrated that CKIP‑1 was the target gene of miR‑98‑5p. miR‑98‑5p was upregulated as a result of treatment with miR‑98‑5p agomir and promoted osteoblast differentiation. Conversely, miR‑98‑5p antagomir inhibited miR‑98‑5p expression and osteoblast differentiation. miR‑98‑5p targeted CKIP‑1 by binding to its 3'‑untranslated region. Furthermore, miR‑98‑5p overexpression decreased the protein levels of CKIP‑1 and inhibition of miR‑98‑5p increased the protein levels of CKIP‑1. The results of the present study indicated that CKIP‑1 was a target gene of miR‑98‑5p and that miR‑98‑5p regulated osteoblast differentiation in MC3T3‑E1 cells by targeting CKIP‑1.

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Section: Discussionmentioning

confidence: 99%

miR‑98‑5p promotes osteoblast differentiation in MC3T3‑E1 cells by targeting CKIP‑1

et al. 2018

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“…The PH domain-containing casein kinase 2 interacting protein-1 (CKIP-1) was first identified as an interactive protein of casein kinase 2a (Bosc et al, 2000 ), and functions as a scaffold protein integrating multiple signaling pathways and is highly expressed in the heart under physiological functions (Ling et al, 2012 ). CKIP-1 was implicated in tumor cell proliferation (Zhu et al, 2017 ), muscle cell differentiation (Safi et al, 2004 ), cell apoptosis (Zhang et al, 2005 ), the regulation of cell morphology (Canton et al, 2006 ), and the actin cytoskeleton (Canton et al, 2005 ). We previously showed that CKIP-1 functioned as a novel regulator of pathological cardiac remodeling induced by pressure overload (Ling et al, 2012 ).…”

Section: Introductionmentioning

confidence: 99%

Myocardial CKIP-1 Overexpression Protects from Simulated Microgravity-Induced Cardiac Remodeling

et al. 2018

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Human cardiovascular system has adapted to Earth's gravity of 1G. The microgravity during space flight can induce cardiac remodeling and decline of cardiac function. At present, the mechanism of cardiac remodeling induced by microgravity remains to be disclosed. Casein kinase-2 interacting protein-1 (CKIP-1) is an important inhibitor of pressure-overload induced cardiac remodeling by decreasing the phosphorylation level of HDAC4. However, the role of CKIP-1 in the cardiac remodeling induced by microgravity is unknown. The purpose of this study was to determine whether CKIP-1 was also involved in the regulation of cardiac remodeling induced by microgravity. We first detected the expression of CKIP-1 in the heart from mice and monkey after simulated microgravity using Q-PCR and western blotting. Then, myocardial specific CKIP-1 transgenic (TG) and wild type mice were hindlimb-suspended (HU) to simulate microgravity effect. We estimated the cardiac remodeling in morphology and function by histological analysis and echocardiography. Finally, we detected the phosphorylation of AMPK, ERK1/2, and HDAC4 in the heart from wild type and CKIP-1 transgenic mice after HU. The results revealed the reduced expression of CKIP-1 in the heart both from mice and monkey after simulated microgravity. Myocardial CKIP-1 overexpression protected from simulated microgravity-induced decline of cardiac function and loss of left ventricular mass. Histological analysis demonstrated CKIP-1 TG inhibited the decreases in the size of individual cardiomyocytes of mice after hindlimb unloading. CKIP-1 TG can inhibit the activation of HDAC4 and ERK1/2 and the inactivation of AMPK in heart of mice induced by simulated microgravity. These results demonstrated CKIP-1 was a suppressor of cardiac remodeling induced by simulated microgravity.

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“…9 CKIP-1 might function as a potential tumour suppressor gene in these malignancies. 5,8,9 In contrast to these previous reports, another study demonstrated that CKIP-1 mRNA was highly expressed in non-small cell lung cancer tissue and that CKIP-1 knockdown could promote cell apoptosis and inhibit tumour cell growth. 7 Although CKIP-1 has been studied in several types of tumour, the expression levels and the possible role of CKIP-1 in the intestinal type of GC remains unclear.…”

Section: Discussionmentioning

confidence: 59%

“…[14][15][16] Recently, the role of CKIP-1 in malignancies has attracted more attention. For example, studies have shown that CKIP-1 is a scaffold protein that may be involved in the tumorigenesis and progression of colorectal cancer, 5 non-Hodgkin's lymphoma 8 and glioma. 9 CKIP-1 might function as a potential tumour suppressor gene in these malignancies.…”

Section: Discussionmentioning

confidence: 99%

High expression of the CKIP-1 gene might promote apoptosis through downregulation of the Ras/ERK signalling pathway in the intestinal type of gastric cancer

Cao

et al. 2020

J Int Med Res

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Objective: To investigate the effect of the casein kinase 2 interacting protein 1 (CKIP-1) on the apoptosis of the intestinal type of gastric cancer (GC). Methods: The levels of CKIP-1 protein and the rates of apoptosis were measured in tissue samples of the intestinal type of GC and human GC cell lines. The rate of apoptosis and the protein levels of B cell lymphoma-2 (Bcl-2), Bcl-2 associated X protein (Bax), cleaved cysteinyl aspartate specific protease 3 (cleaved caspase-3), cleaved caspase-9, rat sarcoma (Ras), extracellular signal-regulated kinase 1 and 2 (ERK1/2) and phosphorylated extracellular signal-regulated kinase 1 and 2 (p-ERK1/2) were analysed in SGC7901 cells expressing CKIP-1 short hairpin RNA (shRNA; knockdown) and SGC7901 cells overexpressing CKIP-1. Results: The levels of CKIP-1 protein were significantly lower in the intestinal type of GC tissues compared with the samples of intestinal metaplasia. Both the levels of CKIP-1 protein and the levels of apoptosis decreased gradually with decreasing cell differentiation in the intestinal type of GC tissue and cell lines; and they were positively correlated. In the CKIP-1 shRNA group, the rate of apoptosis and the levels of Bax, cleaved caspase-3 and cleaved caspase-9 were decreased; and the levels of Bcl-2, Ras and the ratio of p-ERK/ERK were increased, compared with the control group. Opposite results were observed in the CKIP-1 overexpression group.

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Silencing of CKIP-1 promotes tumor proliferation and cell adhesion-mediated drug resistance via regulating AKT activity in non-Hodgkins lymphoma

Cited by 17 publications

References 30 publications

miR‑98‑5p promotes osteoblast differentiation in MC3T3‑E1 cells by targeting CKIP‑1

miR‑98‑5p promotes osteoblast differentiation in MC3T3‑E1 cells by targeting CKIP‑1

Myocardial CKIP-1 Overexpression Protects from Simulated Microgravity-Induced Cardiac Remodeling

High expression of the CKIP-1 gene might promote apoptosis through downregulation of the Ras/ERK signalling pathway in the intestinal type of gastric cancer

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