RETRACTED ARTICLE: Syndecan-1 suppresses cell growth and migration via blocking JAK1/STAT3 and Ras/Raf/MEK/ERK pathways in human colorectal carcinoma cells

Shaojun Wang,Xiaofei Zhang,Guimei Wang,Bin Cao,Hong Yang,Lipeng Jin,Mingjuan Cui,Yongjun Mao

doi:10.1186/s12885-019-6381-y

Abstract

BackgroundSyndecan-1 (SDC-1) is a crucial membrane proteoglycan, which is confirmed to participate in several tumor cell biological processes. However, the biological significance of SDC-1 in colorectal carcinoma is not yet clear. An objective of this study was to investigate the role of SDC-1 in colorectal carcinoma cells.MethodsExpression of SDC-1 in colorectal carcinoma tissues was evaluated by Reverse transcription-quantitative real-time PCR (RT-qPCR) and western blot. After transfection with pcDNA3.1 or pc-SDC-1, the transfection efficiency was measured. Next, SW480, SW620 and LOVO cell viability, apoptosis, migration and adhesion were assessed to explore the effects of exogenous overexpressed SDC-1 on colorectal carcinoma. In addition, the influences of aberrant expressed SDC-1 in Janus kinase 1 (JAK1)/signal transducer and activator of transcription 3 (STAT3) and rat sarcoma virus (Ras)/rapidly accelerated fibrosarcoma (Raf)/mitogen-activated protein kinase (MEK)/extracellular signal-regulated kinase (ERK) pathways were detected by western blot analysis.ResultsSDC-1 mRNA and protein levels were down-regulated in human colorectal carcinoma tissues. SDC-1 overexpression inhibited cell proliferation via suppressing CyclinD1 and c-Myc expression, meanwhile stimulated cell apoptosis via increasing the expression levels of B-cell lymphoma-2-associated x (Bax) and Cleaved-Caspase-3. Additionally, SDC-1 overexpression restrained cell migration via inhibiting the protein expression of matrix metallopeptidase 9 (MMP-9), and elicited cell adhesion through increasing intercellular cell adhesion molecule-1 (ICAM-1). Furthermore, SDC-1 overexpression suppressed JAK1/STAT3 and Ras/Raf/MEK/ERK-related protein levels.ConclusionsIn general, the evidence from this study suggested that SDC-1 suppressed cell growth, migration through blocking JAK1/STAT3 and Ras/Raf/MEK/ERK pathways in human colorectal carcinoma cells.

Highlights

Syndecan-1 (SDC-1) is a crucial membrane proteoglycan, which is confirmed to participate in several tumor cell biological processes
In general, the evidence from this study suggested that SDC-1 suppressed cell growth, migration through blocking Janus kinase 1 (JAK1)/signal transducer and activator of transcription 3 (STAT3) and rat sarcoma virus (Ras)/rapidly accelerated fibrosarcoma (Raf)/mitogen-activated protein kinase (MEK)/extracellular signal-regulated kinase (ERK) pathways in human colorectal carcinoma cells
SDC-1 was down-expressed in human colorectal carcinoma tissues First of all, we examined SDC-1 expression in human colorectal carcinoma tissues by Reverse transcription-quantitative real-time PCR (RT-qPCR)

Summary

Introduction

Syndecan-1 (SDC-1) is a crucial membrane proteoglycan, which is confirmed to participate in several tumor cell biological processes. Syndecan-1 (SDC1), the most crucial membrane proteoglycan, is implicated in several cellular processes, such as cell-extracellular matrix interactions [6], growth factor [7], integrin activity [8], migration [9] and inflammatory response [10]. A clinic pathological study showed that epithelial SDC-1-positive was significantly associated with tumor size in human colorectal carcinoma [14]. Immunohistochemical research such as that conducted by Yosuke et al shown that there was unambiguous relativity between loss of SDC-1 and poor prognosis of colorectal carcinoma patients [15]. There is no data on the possible role of SDC-1 in human colorectal carcinoma

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