Department of Maxillofacial Surgery, Stomatological Hospital, Jiamusi University, Jiamusi 154002, Heilongjiang, China.
Basic Medical College, Jiamusi University, Jiamusi 154002, Heilongjiang, China.
Biosci Rep. 2021 Dec 22;41(12). doi: 10.1042/BSR20212403.
CXCL3 plays extensive roles in tumorigenesis in various types of human cancers through its roles in tumor cell differentiation, invasion, and migration. However, the mechanisms of CXCL3 in head and neck squamous cell carcinoma (HNSCC) remain unclear. In our study, multiple databases were used to explore the expression level, prognostic value, and related mechanisms of CXCL3 in human HNSCC through bioinformatic methods. We also performed further experiments in vivo and in vitro to evaluate the expression of CXCL3 in a human head and neck tissue microarray and the underlying effect mechanisms of CXCL3 on the tumor biology of HNSCC tumor cells. The result showed that the expression level of CXCL3 in patients with HNSCC was significantly higher as compared with that in normal tissues (P<0.05). Kaplan-Meier survival analysis demonstrated that patients with high CXCL3 expression had a lower overall survival rate (P=0.038). CXCL3 was further identified as an independent prognostic factor for HNSCC patients by Cox regression analysis, and GSEA exhibited that several signaling pathways including Apoptosis, Toll-like receptor, Nod-like receptor, Jak-STAT, and MAPK signaling pathways may be involved in the tumorigenesis of HNSCC. CAL27 cells overexpressing or HNSCC cells treated with exogenous CXCL3 exhibited enhanced cell malignant behaviors, whereas down-regulating CXCL3 expression resulted in decreased malignant behaviors in HSC4 cells. In addition, CXCL3 may affect the expression of several genes, including ERK1/2, Bcl-2, Bax, STAT3, and NF-κB. In summary, our bioinformatics and experiment findings effectively suggest the information of CXCL3 expression, roles, and the potential regulatory network in HNSCC.
CXCL3 通过其在肿瘤细胞分化、侵袭和迁移中的作用,在多种人类癌症的发生中发挥广泛作用。然而,CXCL3 在头颈部鳞状细胞癌(HNSCC)中的机制尚不清楚。在我们的研究中,通过生物信息学方法,使用多个数据库探索了 CXCL3 在人类 HNSCC 中的表达水平、预后价值和相关机制。我们还在体内和体外进行了进一步的实验,以评估 CXCL3 在人类头颈部组织微阵列中的表达及其对 HNSCC 肿瘤细胞肿瘤生物学的潜在影响机制。结果表明,HNSCC 患者 CXCL3 的表达水平明显高于正常组织(P<0.05)。Kaplan-Meier 生存分析表明,高 CXCL3 表达的患者总体生存率较低(P=0.038)。Cox 回归分析进一步将 CXCL3 鉴定为 HNSCC 患者的独立预后因素,GSEA 显示包括细胞凋亡、Toll 样受体、Nod 样受体、Jak-STAT 和 MAPK 信号通路在内的几种信号通路可能参与 HNSCC 的发生。CAL27 细胞过表达或 HNSCC 细胞用外源性 CXCL3 处理后表现出增强的细胞恶性行为,而下调 CXCL3 表达则导致 HSC4 细胞的恶性行为减少。此外,CXCL3 可能影响包括 ERK1/2、Bcl-2、Bax、STAT3 和 NF-κB 在内的几种基因的表达。总之,我们的生物信息学和实验结果有效地提供了 CXCL3 在 HNSCC 中的表达、作用和潜在调控网络的信息。