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CXCL3 overexpression promotes the tumorigenic potential of uterine cervical cancer cells via the MAPK/ERK pathway |
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| Authors: | Ya-Ling Qi Yue Li Xia-Xia Man Hong-Yu Sui Xiao-Lian Zhao Peng-Xia Zhang Xiu-Sheng Qu Hui Zhang Bai-Xin Wang Jing Li Shu-Fang Qi Lin-Lin Jia Hai-Yan Luan Chun-Bin Zhang Wei-Qun Wang |
| Affiliation: | 1. Basic Medical College, Jiamusi University, Jiamusi, Heilongjiang, China Department of Histology and Embryology, Hainan Medical College, Haikou, Hainan, China Ya-Ling Qi, Yue Li, and Xia-Xia Man contributed equally to this work.;2. Basic Medical College, Jiamusi University, Jiamusi, Heilongjiang, China Ya-Ling Qi, Yue Li, and Xia-Xia Man contributed equally to this work.;3. Department of Oncologic Gynecology, First Hospital of Jilin University, Changchun, Jilin, China Ya-Ling Qi, Yue Li, and Xia-Xia Man contributed equally to this work.;4. Basic Medical College, Jiamusi University, Jiamusi, Heilongjiang, China;5. First Affiliated Hospital, Jiamusi University, Jiamusi, Heilongjiang, China |
| Abstract: | CXCL3 belongs to the CXC-type chemokine family and is known to play a multifaceted role in various human malignancies. While its clinical significance and mechanisms of action in uterine cervical cancer (UCC) remain unclear. This investigation demonstrated that the UCC cell line HeLa expressed CXCL3, and strong expression of CXCL3 was detected in UCC tissues relative to nontumor tissues. In addition, CXCL3 expression was strongly correlated with CXCL5 expression in UCC tissues. In vitro, HeLa cells overexpressing CXCL3, HeLa cells treated with exogenous CXCL3 or treated with conditioned medium from WPMY cells overexpressing CXCL3, exhibited enhanced proliferation and migration activities. In agreement with these findings, CXCL3 overexpression was also associated with the generation of HeLa cell tumor xenografts in athymic nude mice. Subsequent mechanistic studies demonstrated that CXCL3 overexpressing influenced the expression of extracellular signal-regulated kinase (ERK) signaling pathway associated genes, including ERK1/2, Bcl-2, and Bax, whereas the CXCL3-induced proliferation and migration effects were attenuated by exogenous administration of the ERK1/2 blocker PD98059. The data of the current investigation support that CXCL3 appears to hold promise as a potential tumor marker and interference target for UCC. |
| Keywords: | cervical cancer CXCL3 ERK malignant behavior upregulation |