College of Life Sciences, Henan Agricultural University, Zhengzhou 450002, China.
Int J Mol Sci. 2023 Jun 26;24(13):10652. doi: 10.3390/ijms241310652.
Ovarian cancer is a gynecological tumor with an incidence rate lower than those of other gynecological tumor types and the second-highest death rate. CC chemokine 2 (CCL2) is a multifunctional factor associated with the progression of numerous cancers. However, the effect of CCL2 on ovarian cancer progression is unclear. Here, we found that exogenous CCL2 and the overexpression of CCL2 promoted the proliferation and metastasis of ovarian cancer cells. On the other hand, CCL2 knockdown via CRISPR/Cas9 inhibited ovarian cancer cell proliferation, migration, and invasion. The present study demonstrated that mitogen-activated protein three kinase 19 (MAP3K19) was the key CCL2 target for regulating ovarian cancer progression through transcriptome sequencing. Additionally, MAP3K19 knockout inhibited ovarian cancer cell proliferation, migration, and invasion. Furthermore, CCL2 increased MAP3K19 expression by activating the mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) pathway. The present study showed the correlation between CCL2 and ovarian cancer, suggesting that CCL2 may be a novel target for ovarian cancer therapy.
卵巢癌是一种妇科肿瘤，其发病率低于其他妇科肿瘤类型，死亡率却位居第二。CC 趋化因子 2（CCL2）是一种与多种癌症进展相关的多功能因子。然而，CCL2 对卵巢癌进展的影响尚不清楚。本研究发现外源性 CCL2 和 CCL2 的过表达促进了卵巢癌细胞的增殖和转移。另一方面，通过 CRISPR/Cas9 敲低 CCL2 抑制了卵巢癌细胞的增殖、迁移和侵袭。本研究通过转录组测序证明，丝裂原活化蛋白激酶 19（MAP3K19）是 CCL2 调节卵巢癌进展的关键靶点。此外，MAP3K19 敲除抑制了卵巢癌细胞的增殖、迁移和侵袭。此外，CCL2 通过激活丝裂原活化蛋白激酶激酶（MEK）/细胞外信号调节激酶（ERK）通路增加 MAP3K19 的表达。本研究表明 CCL2 与卵巢癌之间存在相关性，提示 CCL2 可能是卵巢癌治疗的新靶点。
