Polo-like kinase 1 is overexpressed in renal cancer and participates in the proliferation and invasion of renal cancer cells

Abstract

Polo-like kinase 1 (Plk1) is an interesting molecule both as a biomarker and as a target for highly specific cancer therapy for several reasons. However, the functional significance of Plk1 in renal cell carcinoma (RCC) has not been reported. To explore whether Plk1 plays a general role in renal carcinoma, we examined the expression of Plk1 protein in renal urothelial carcinoma and cell lines, and analyzed the relationship between Plk1 protein expression and development, proliferation, and invasion of renal carcinoma. Immunohistochemisty was used to detect the expression of Plk1 in 100 renal carcinoma tissues. Moreover, the expression of Plk1 was analyzed by western blot and real-time polymerase chain reaction (PCR) in 80 renal carcinoma tissues and 20 normal renal tissues. CCK-8 assay, colony formation assay, and Transwell assay were used to examine proliferation and invasion ability of renal cancer cells with treatment of scytonemin (the specific inhibitor of Plk1). Statistical analysis was used to discuss the association between Plk1 expression and clinicopathologic parameters, and proliferation and invasion ability of renal cancer cells. Plk1 expressions were greater in cancerous tissues than in normal tissues (P<0.05). With an increase in tumor grade and stage, tumor metastasis, and recurrence, the level of Plk1 increased significantly in renal cancerous tissues. Moreover, there was a significantly higher expression of Plk1 in higher degree of malignant renal adenocarcinoma cell ACHN than that in renal adenocarcinoma cell 769-P. With increasing concentration of scytonemin, we found that cell proliferation and invasion activity decreased significantly. Plk1 expression status was closely correlated with important histopathologic characteristics (grades, stages, metastasis, and recurrence) of renal carcinomas. Furthermore, Plk1 played an important function on renal cancer cells' proliferation and invasion.

FOXM1 participates in PLK1-regulated cell cycle progression in renal cell cancer cells

“…the 769-P and ACHN cells transfected with PLK1 siRNA demonstrated an increased percentage of cells in the G2/M phase, which supports the findings of previous studies (8,9). A previous study reported that PLK1 was important for the proliferation of bladder cancer cells by regulating the cancer cell cycle between the G1/S and G2/M phases (9).…”

“…However, the possible heterogeneity of kidney tumors may make the identification of specific markers more challenging. A previous study revealed that PLK1 is overexpressed in renal cancer and participates in the proliferation and invasion of renal cancer cells (8). Although the evidence has elucidated the importance of PLK1 as a tumor promoter in renal cell carcinoma, the precise molecular mechanisms remain largely unknown.…”

“…The serine/threonine kinase PLK1 governs several mitotic stages, including entry into mitosis, centrosome maturation, bipolar spindle assembly, activation of the anaphase-promoting complex/cyclosome by phosphorylation of early mitotic inhibitor 1, chromosome segregation and mitotic exit (4). The overexpression of PLK1 is associated with a poor prognosis in a variety of cancers (5)(6)(7)(8)(9). Beyond the regulation of mitosis, PLK1 possesses cancer cell-specific functions in G1/S transition and DNA replication (10,11).…”

Targeting polo-like kinase 1 by NMS-P937 in osteosarcoma cell lines inhibits tumor cell growth and partially overcomes drug resistance

“…Finally, we proved that NMS-P937 treatment significantly suppresses both clonogenic and migration ability of OS cells, which is highly relevant as it has been suggested that in other neoplasms PLK1 is involved in metastatic dissemination and malignancy [34][35][36].…”

Plk1 inhibition leads to a failure of mitotic division during the first mitotic division in pig embryos

“…In human somatic cells, inhibited Plk1 leads to multiple mitotic defects, including the formation of abnormal spindles, misaligned chromosomes and i mproper chromosom e condensation [10]. Additionally, up-or downregulation of Plk1 can induce a variety of human tumor cells or mouse embryonic cell mitotic defects, causing aneuploidy or cancer [11][12][13]. This study shows that Plk1 might play a critical role in the process of bipolar spindle assembly and chromosome arrangement during mitosis in somatic cells.…”