Department of Gastroenterology, The Affiliated Hospital of Qingdao University, Qingdao, 266000, China.
Department of Geriatrics, The Affiliated Hospital of Qingdao University, No.59 Haier Road, Laoshan District, Qingdao, 266000, Shandong, China.
BMC Cancer. 2019 Nov 29;19(1):1160. doi: 10.1186/s12885-019-6381-y.
Syndecan-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.
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.
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.
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.
硫酸乙酰肝素蛋白聚糖-1（SDC-1）是一种重要的膜蛋白聚糖，已被证实参与多种肿瘤细胞的生物学过程。然而，SDC-1 在结直肠癌中的生物学意义尚不清楚。本研究旨在探讨 SDC-1 在结直肠癌细胞中的作用。
采用逆转录定量实时 PCR（RT-qPCR）和 Western blot 检测结直肠癌组织中 SDC-1 的表达。转染 pcDNA3.1 或 pc-SDC-1 后，测量转染效率。然后，评估 SW480、SW620 和 LOVO 细胞的活力、凋亡、迁移和黏附，以探讨外源性过表达 SDC-1 对结直肠癌的影响。此外，通过 Western blot 分析检测异常表达的 SDC-1 对 Janus 激酶 1（JAK1）/信号转导和转录激活因子 3（STAT3）和大鼠肉瘤病毒（Ras）/快速加速纤维肉瘤（Raf）/丝裂原活化蛋白激酶（MEK）/细胞外信号调节激酶（ERK）通路的影响。
人结直肠癌组织中 SDC-1 mRNA 和蛋白水平下调。SDC-1 过表达通过抑制细胞周期蛋白 D1 和 c-Myc 的表达抑制细胞增殖，同时通过增加 B 细胞淋巴瘤-2 相关 X（Bax）和Cleaved-Caspase-3 的表达水平刺激细胞凋亡。此外，SDC-1 过表达通过抑制基质金属蛋白酶 9（MMP-9）的蛋白表达抑制细胞迁移，并通过增加细胞间黏附分子-1（ICAM-1）的表达诱导细胞黏附。此外，SDC-1 过表达抑制 JAK1/STAT3 和 Ras/Raf/MEK/ERK 相关蛋白水平。
总之，本研究结果表明，SDC-1 通过阻断 JAK1/STAT3 和 Ras/Raf/MEK/ERK 通路抑制人结直肠癌细胞的生长和迁移。
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