*** em p /em ? ?0.001. 12885_2019_6381_MOESM2_ESM.tif (1.0M) GUID:?2C1ADB19-3F78-4DED-878C-48FDBC14FC04 Additional file 3: Physique S3. and ICAM-1. -actin was used as an internal reference for normalizing the protein expression. *** em p /em ? ?0.001. 12885_2019_6381_MOESM2_ESM.tif (1.0M) GUID:?2C1ADB19-3F78-4DED-878C-48FDBC14FC04 Additional file 3: Figure S3. SDC-1 inhibited the phosphorylation of Ras/Raf/MEK/ERK pathway. pcDNA3.1 or pc-SDC-1 was transfected into LOVO cells. (A-B) Western blot analysis was utilized to evaluate the protein levels of Ras, Raf, p-MEK and p-ERK. -actin was used as an internal reference for normalizing the protein expression. *** AZ191 em p /em ? ?0.001. 12885_2019_6381_MOESM3_ESM.tif (1.7M) GUID:?8C5D5499-87C3-4E43-9817-8FBF9E96390F Data Availability StatementThe datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request. Abstract Background Syndecan-1 (SDC-1) is usually a crucial membrane proteoglycan, which is usually 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. Methods Expression 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. Results SDC-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. Conclusions In 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. strong class=”kwd-title” Keywords: Syndecan-1, Colorectal carcinoma, Migration, JAK1/STAT3, Ras/Raf/MEK/ERK Background Colorectal carcinoma is one of the most common malignancies of alimentary canal, which arises from the colon or the junction of the rectum and sigmoid colon. Colorectal carcinoma is generally unrecognized with symptomless in the early stage or is seen with ordinary symptoms in cancer metaphase, such as bloating and indigestion. With growing new cases being diagnosed all around the world every year, colorectal carcinoma is known to be one of the most critical popular diseases, accompanying by a high malignant degree and mortality [1]. Surgical operation and chemotherapy have been developed for the treatment of colorectal carcinoma [2, 3]. Nevertheless, there has been no satisfactory change in ATP7B the patients survival rate, especially for colorectal carcinoma patients with cancer metastasis which was? the dominating cause for poor survival and prognosis of patients [4]. Thus, it is urgent to explore novel targets that may provide potential resolutions for metastasis in colorectal carcinoma cells. AZ191 Heparan sulfate proteoglycan (HSPG) is usually a kind of?heparan sulfate (HS)-bonding glycoproteins [5]. Syndecan-1 (SDC-1), the most crucial membrane proteoglycan, is usually implicated in several cellular processes, such as cell-extracellular matrix interactions [6], growth factor [7], integrin activity [8], migration [9] and inflammatory response [10]. Furthermore, there is growing evidence that SDC-1 participates in the development of tumor progression. For instance, recent evidence suggested that silencing SDC-1 led to cell apoptosis of human urothelial carcinoma [11]. SDC-1 was believed to modulate the cancer stem cell phenotype via regulating inflammatory cytokines in breast cancer [12]. Beyond that, SDC-1 functioned in epithelial-mesenchymal transition and migratory ability in human oral carcinomatosis [13]. A clinic pathological study AZ191 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 AZ191 patients [15]. However, there is no data around the possible role of SDC-1 in human colorectal carcinoma. In this paper, we verified the mRNA and protein expression of SDC-1 in human colorectal carcinoma tissues and focused on the biological cellular effects of SDC-1 on human colorectal carcinoma cell lines (SW620, SW480 and.

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