Department of Colorectal Surgery, General Hospital of Ningxia Medical University, Yinchuan 750003, China.
College of Clinical Medicine, Ningxia Medical University, Yinchuan 750004, China.
Contrast Media Mol Imaging. 2022 Jul 12;2022:2387192. doi: 10.1155/2022/2387192. eCollection 2022.
Chemokine C-C motif chemokine ligand 3 (CCL3) plays an important role in the invasion and metastasis of malignant tumors. For developing new therapeutic targets and antitumor drugs, the effect of chemokine CCL3 and the related cytokine network on colorectal cancer should be investigated. This study used cell, tissue, and animal experiments to prove that CCL3 is highly expressed in colorectal cancer and confirmed that CCL3 can promote the proliferation of cancer cells, and its expression is closely related to TRAF6/NF-B molecular pathway. In addition, protein chip technology was used to examine colorectal cancer tissue samples and identify the key factors of chemokine CCL3 and the toll-like receptors/nuclear factor-B (TLR/NF-B) pathway in cancer and metastatic lymph nodes. Furthermore, the lentiviral vector technology was employed for transfection to construct interference and overexpression cell lines. The experimental results reveal the mechanism of CCL3 and TNF receptor-associated factor 6 (TRAF6)/NF-B pathway-related factors and their effects on the proliferation of colon cancer cells. Finally, the expression and significance of CCL3 in colorectal cancer tissues and its correlation with clinical pathology were studied by immunohistochemistry. Also, the results confirmed that CCL3 and C-C motif chemokine receptor 5 (CCR5) were expressed in adjacent tissues, colorectal cancer tissues, and metastatic cancer. The expression level was correlated with the clinical stage and nerve invasion. The expression of chemokine CCL3 and receptor CCR5 was positively correlated with the expression of TRAF6 and NF-B and could promote the proliferation, invasion, and migration of colorectal cancer cells through TRAF6 and NF-B.
趋化因子 C-C 基序趋化因子配体 3（CCL3）在恶性肿瘤的侵袭和转移中发挥重要作用。为了开发新的治疗靶点和抗肿瘤药物，应该研究趋化因子 CCL3 及其相关细胞因子网络对结直肠癌的影响。本研究通过细胞、组织和动物实验证明 CCL3 在结直肠癌中高度表达，并证实 CCL3 可促进癌细胞增殖，其表达与 TRAF6/NF-B 分子途径密切相关。此外，还使用蛋白质芯片技术检测结直肠癌组织样本，并鉴定趋化因子 CCL3 和 Toll 样受体/核因子-B（TLR/NF-B）途径在癌症和转移性淋巴结中的关键因素。此外，还采用慢病毒载体技术进行转染，构建干扰和过表达细胞系。实验结果揭示了 CCL3 和肿瘤坏死因子受体相关因子 6（TRAF6）/NF-B 通路相关因子的作用机制及其对结肠癌细胞增殖的影响。最后，通过免疫组织化学研究 CCL3 在结直肠癌组织中的表达及其与临床病理的关系。此外，结果证实 CCL3 和 C-C 基序趋化因子受体 5（CCR5）在相邻组织、结直肠癌组织和转移性癌组织中表达。表达水平与临床分期和神经浸润相关。趋化因子 CCL3 和受体 CCR5 的表达与 TRAF6 和 NF-B 的表达呈正相关，并可通过 TRAF6 和 NF-B 促进结直肠癌细胞的增殖、侵袭和迁移。
