Panoply™ Human NEK2 Knockdown Stable Cell Line

NEK2, a serine/threonine kinase involved in mitosis, has been found to be associated with chromosomal instability, tumor progression, and metastasis, but its role in cervical cancer radioresistance remains unclear. Here, researchers found that NEK2 protein levels are overexpressed in cervical cancer tissues and are positively correlated with tumor stage and lymph node metastasis. Furthermore, NEK2 deficiency inhibits cervical cancer development and progression and enhances its radiosensitivity. Through RNA sequencing, researchers identified Wnt1 as a key downstream effector of NEK2. Knockdown of NEK2 reduced Wnt1 mRNA and protein levels, thereby inhibiting the activation of the Wnt/β-catenin signaling pathway. More importantly, overexpression of Wnt1 could partially reverse these consequences of NEK2 deficiency in cervical cancer cells. These results suggest that NEK2 activates the Wnt/β-catenin signaling pathway through Wnt1, thereby driving tumorigenesis and radioresistance in cervical cancer, indicating that NEK2 may be a promising target for radiosensitization in cervical cancer.

To further confirm the role of NEK2 in the development and progression of cervical cancer, researchers constructed stable NEK2-knockdown SiHa cells (Figure 1a). They found that the growth and proliferation of NEK2-knockdown cervical cancer cells were significantly inhibited (Figures 1b and 1c). To investigate whether NEK2 drives tumorigenesis in vivo, researchers subcutaneously implanted control cells or NEK2-knockdown cells into T-cell-deficient athymic nude mice. As shown in Figures 1d-f, compared with the control group, the tumor volume and weight of the NEK2-knockdown group were significantly reduced. In summary, these studies indicate that NEK2 deficiency inhibits the development and progression of cervical cancer both in vitro and in vivo.

Figure 1. Downregulation of NEK2 inhibited the oncogenic behavior of cervical cancer cells in vitro and in vivo. (Xu T, et al., 2020)