CIAPIN1 gene silencing enhances chemosensitivity in a drug-resistant animal model in vivo

Wang, X.M.; Gao, Si; Guo, Xiaofei; Sun, Weizheng; Yan, Zhaoqi; Wang, W.X.; Xu, Yi; Lü, Dan

doi:10.1590/1414-431x20133356

Cited by 5 publications

(5 citation statements)

References 25 publications

(39 reference statements)

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“…Although the alteration of CIAPIN1 regulated proliferative and migrative marker in VSMC it was reported that there was an association between CIAPIN1 and multidrug resistance in cancer , not significant (Lu et al, 2012;X. M. Wang et al, 2014), the underlying molecular mechanism remains unclear.…”

Section: Interaction Between Ciapin1 and P53 Signallingmentioning

confidence: 98%

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Cytokine‐induced apoptosis inhibitor 1 (CIAPIN1) accelerates vascular remodelling via p53 and JAK2‐STAT3 regulation in vascular smooth muscle cells

Han

Heo

Myung

2021

British J Pharmacology

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Background and purpose: Abnormal vascular smooth muscle cell (VSMC) proliferation and migration lead to neointima formation, which eventually results in cardiovascular hyperplastic diseases. The molecular mechanisms underlying these cellular processes have not been fully understood. Cytokine-induced apoptosis inhibitor 1 (CIAPIN1) has been identified as an anti-apoptotic molecule, but little is known about its target genes and related pathways in VSMC dysfunction or its clinical implication in neointima formation following vascular injury.Experimental approach: Determination, using loss/gain-of-function approaches by gene delivery, of whether CIAPIN1 modulates VSMC proliferation, migration and neointima formation and the underlying mechanisms was carried out. Balloon injury or ligation and local delivery of lentivirus were performed on rat or mouse carotid arteries. Rat aortic smooth muscle cells, the primary cell, was used as the model to evaluate the effect of CIAPIN1 on proliferation and migration.Key results: CIAPIN1 was overexpressed in the neointimal region of rat arteries.CIAPIN1 deficiency markedly inhibited injury-induced or ligation-induced intimal hyperplasia and suppressed PDGF-BB-induced VSMC proliferation, migration and cell cycle progression, while overexpression promoted proliferation, migration and neointima formation. CIAPIN1 negatively regulated Tp53 transcription, which promoted cell cycle progression and migration via cyclin E1-CDK2/pRb/PCNA and the MMP2 pathway. CIAPIN1 also increased JAK2 expression, enhancing JAK2 and STAT3 phosphorylation by vascular injury, which forced phenotypic switching from contractile to synthetic state in injured arteries.Conclusions and implications: These findings provide new insights into the mechanism by which CIAPIN1 regulates vascular remodelling and suggest a novel therapeutic target for treating vascular proliferative diseases.

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Section: Interaction Between Ciapin1 and P53 Signallingmentioning

confidence: 98%

“…Li et al, 2010) by affecting the ATP binding cassette subfamily B member 1 (ABCB1) (Y. F. Zhang et al, 2011), sensitising drug actions (J. Wang et al, 2016;X. M. Wang et al, 2014), cell growth and proliferation (Huang et al, 2017;X.…”

Section: Introductionmentioning

confidence: 99%

Cytokine‐induced apoptosis inhibitor 1 (CIAPIN1) accelerates vascular remodelling via p53 and JAK2‐STAT3 regulation in vascular smooth muscle cells

Han

Heo

Myung

2021

British J Pharmacology

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“…In terms of multidrug resistance, Wang et al reported that overexpression of CIAPIN1 contributes to multidrug resistance (MDR) in breast cancer. CIAPIN1 gene silencing enhanced the sensitivity of tumor cells to doxorubicin in drug-resistant breast cancer xenografts in this nude mouse model [39]. Moreover, Lu et al showed that, in the MCF7/ADM cell line of breast cancer, CIAPIN1 gene silencing by siRNA reduced the drug resistance against epirubicin, paclitaxel, and gemcitabine by regulating MDR1 and P53 expression [40].…”

Section: Discussionmentioning

confidence: 84%

Prediction of CIAPIN1 (Cytokine-Induced Apoptosis Inhibitor 1) Signaling Pathway and Its Role in Cholangiocarcinoma Metastasis

Truong

Wongwattanakul

Proungvitaya

et al. 2022

JCM

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Cholangiocarcinoma (CCA), a malignancy of the biliary epithelium, can arise at any point in the biliary system. We previously reported that CIAPIN1 is detectable in the sera and that its overexpression was associated with poor prognosis and metastasis of CCA patients. In this study, we investigated further its expression in CCA tissues, biological functions, and related signaling pathways in CCA cells. First, we examined CIAPIN1 expression in CCA tissues of 39 CCA patients using immunohistochemistry (IHC). Then, CIAPIN1-related proteins expressed in CCA cells were identified using RNA interference (siRNA) and liquid chromatography–mass spectrometry (LC–MS/MS). To predict the functions and signaling pathways of CIAPIN1 in CCA cells, the identified proteins were analyzed using bioinformatics tools. Then, to validate the biological functions of CIAPIN1 in the CCA cell line, transwell migration/invasion assays were used. CIAPIN1 was overexpressed in CCA tissues compared with adjacent noncancerous tissues. Its overexpression was correlated with lymph node metastasis. Bioinformatic analyses predicted that CIAPIN1 is connected to the TGF-β/SMADs signaling pathway via nitric oxide synthase 1 (NOS1) and is involved in the metastasis of CCA cells. In fact, cell migration and invasion activities of the KKU-100 CCA cell line were significantly suppressed by CIAPIN1 gene silencing. Our results unravel its novel function and potential signaling pathway in metastasis of CCA cells. CIAPIN1 can be a poor prognostic factor and can be a promising target molecule for CCA chemotherapy.

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“…Thus, CIAPIN1 is a potential target for the improvement of therapeutic efficacy. In a study using nude mice with MDR breast cancer tumors, the combination of chemotherapy with the knockdown of CIAPIN1 levels using lentivirus-vector-based RNAi significantly inhibited tumor growth in vivo ( 19 ). In agreement with these previous studies, the present results demonstrated that CIAPIN1 protein levels significantly increased in TDR breast cancer cells.…”

Section: Discussionmentioning

confidence: 99%

Upregulation of microRNA-143 reverses drug resistance in human breast cancer cells via inhibition of cytokine-induced apoptosis inhibitor 1

Wang

et al. 2017

Oncology Letters

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Cytokine-induced apoptosis inhibitor 1 (CIAPIN1), originally termed anamorsin, is an anti-apoptotic molecule that acts as a downstream effector of the receptor tyrosine kinase-Ras signaling pathway. Overexpression of CIAPIN1 contributes to multidrug resistance (MDR) and microRNA (miR)-143 is typically considered a tumor suppressor in breast cancer. The present study aimed to evaluate the therapeutic potential of miR-143 as a treatment for drug-resistant breast cancer via the downregulation of CIAPIN1 in vitro. The expression levels of miR-143 were measured using quantitative polymerase chain reaction and the expression levels of CIAPIN1 were detected via western blot analysis. Bioinformatic analyses was additionally conducted to search for miR-143, which may potentially target CIAPIN1. Luciferase reporter plasmids were created and used to verify direct targeting. In addition, Taxol-induced drug-resistant (TDR) breast cancer cell proliferation was evaluated using the Cell Counting Kit-8 assay in vitro. The present study identified an inverse association between miR-143 and CIAPIN1 protein expression levels in breast cancer MCF-7, MDA-MB-231 and MDA-MB-453 TDR cells. Specific targeting sites for miR-143 in the 3′-untranslated region of the CIAPIN1 gene were identified, which exhibit the ability to regulate CIAPIN1 expression. It was revealed that the repression of CIAPIN1 via miR-143 suppressed the proliferation of breast cancer TDR cells. The findings of the present study verified the role of miR-143 as a tumor suppressor in breast cancer MDR via inhibition of CIAPIN1 translation.

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CIAPIN1 gene silencing enhances chemosensitivity in a drug-resistant animal model in vivo

Cited by 5 publications

References 25 publications

Cytokine‐induced apoptosis inhibitor 1 (CIAPIN1) accelerates vascular remodelling via p53 and JAK2‐STAT3 regulation in vascular smooth muscle cells

Cytokine‐induced apoptosis inhibitor 1 (CIAPIN1) accelerates vascular remodelling via p53 and JAK2‐STAT3 regulation in vascular smooth muscle cells

Prediction of CIAPIN1 (Cytokine-Induced Apoptosis Inhibitor 1) Signaling Pathway and Its Role in Cholangiocarcinoma Metastasis

Upregulation of microRNA-143 reverses drug resistance in human breast cancer cells via inhibition of cytokine-induced apoptosis inhibitor 1

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