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

Zhang, Zhe; Zhang, Guojun; Kong, Chuize

doi:10.3892/ol.2016.4228

Cited by 35 publications

(38 citation statements)

References 29 publications

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“…These results indicate that PLK1 upregulation may be involved in cancer progression and invasion. This is in line with the results of previous studies [60], [61], [62].…”

Section: Plk1 and Human Cancersupporting

confidence: 93%

“…In addition to the tumor suppressors, PLK1 interacts with other classes of genes or proteins such as kinases: AURKA [84], [85], BUB1 [86], [87], and WEE1 [88]; oncogenes: MDM2 [89] and FOXO3 [90]; and transcriptional factors: HSF1 [91], [92], [93], RELA [94], TRIOBP [95], and FOXM1 [62], [96], [97], [98], etc. These interactions may be essential for PLK1 to play an important role in regulation of the cell cycle, and dysfunction of the interactions could be associated with cancer and other diseases.…”

Section: Plk1 and Human Cancermentioning

confidence: 99%

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PLK1, A Potential Target for Cancer Therapy

Liu

Sun

Wang

2017

Translational Oncology

362

269

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Polo-like kinase 1 (PLK1) plays an important role in the initiation, maintenance, and completion of mitosis. Dysfunction of PLK1 may promote cancerous transformation and drive its progression. PLK1 overexpression has been found in a variety of human cancers and was associated with poor prognoses in cancers. Many studies have showed that inhibition of PLK1 could lead to death of cancer cells by interfering with multiple stages of mitosis. Thus, PLK1 is expected to be a potential target for cancer therapy. In this article, we examined PLK1’s structural characteristics, its regulatory roles in cell mitosis, PLK1 expression, and its association with survival prognoses of cancer patients in a wide variety of cancer types, PLK1 interaction networks, and PLK1 inhibitors under investigation. Finally, we discussed the key issues in the development of PLK1-targeted cancer therapy.

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“…These results indicate that PLK1 upregulation may be involved in cancer progression and invasion. This is in line with the results of previous studies [60], [61], [62].…”

Section: Plk1 and Human Cancersupporting

confidence: 93%

Section: Plk1 and Human Cancermentioning

confidence: 99%

PLK1, A Potential Target for Cancer Therapy

Liu

Sun

Wang

2017

Translational Oncology

362

269

View full text Add to dashboard Cite

show abstract

“…FOX transcription factor family, which is named after the forkhead winged-helix DNA-binding domain, 23 has been reported to act as important regulators of numerous biological processes, including cell cycle regulation, proliferation, differentiation, senescence, survival, metabolism and apoptosis. 24,25 A series of FOX genes, such as FOXC2, 26,27 FOXJ1, 28 FOXL1, 29 FOXM1, [30][31][32][33][34][35] and FOXPs, [36][37][38] have been reported to play vital roles in the carcinogenesis, metastasis and prognosis of ccRCC. A previous study reported that FOXK2 expression was elevated in human colorectal cancer and is associated with intestinal tumorigenesis; 20 two other studies reported that FOXK2 was downregulated in breast cancer and suppressed the carcinogenesis of breast cancer.…”

Section: Discussionmentioning

confidence: 99%

FOXK2 suppresses the malignant phenotype and induces apoptosis through inhibition of EGFR in clear‐cell renal cell carcinoma

Zhang

et al. 2018

Intl Journal of Cancer

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Forkhead box K2 (FOXK2) belongs to the forkhead box transcription factor family. Recent studies have revealed that FOXK2 plays essential roles in cancer cell proliferation and survival. However, the biological function of FOXK2 in renal cell carcinoma remains unexplored. In our study, we demonstrated that FOXK2 mRNA and protein levels were decreased in clear-cell renal cell carcinoma (ccRCC) tissues compared to those in corresponding non-tumor renal tissues, and decreased FOXK2 levels were associated with poor prognosis in ccRCC patients after nephrectomy. FOXK2 suppressed proliferation, migration and invasion capabilities of ccRCC cells and induced cellular apoptosis in vitro. Moreover, we found that FOXK2 overexpression inhibited xenograft tumor growth and promoted apoptosis in vivo. Genome-wide transcriptome profiling using FOXK2 overexpressed 769-P cells revealed that the epidermal growth factor receptor (EGFR) was a potential downstream gene of FOXK2. Overexpression of EGFR is able to rescue the inhibited proliferation capacity and the enhanced apoptosis capacity due to the overexpression of FOXK2 in 769-P cells. Collectively, our results indicate that FOXK2 inhibits the malignant phenotype of ccRCC and acts as a tumor suppressor possibly through the inhibition of EGFR.

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“…Recently, overexpression of FOXM1 was correlated with the poor prognosis of patients with malignant tumors and has been reported in many types of cancers including GC (28–32). Zhang et al reported that downregulation of FOXM1 suppressed PLK1-regulated cell cycle progression in renal cancer cells (33). Additionally, Inoguchi et al found that microRNA-24-1 inhibited bladder cancer cell proliferation by targeting FOXM1 (34).…”

Section: Discussionmentioning

confidence: 99%

Tanshinone IIA suppresses gastric cancer cell proliferation and migration by downregulation of FOXM1

Wang

et al. 2017

Oncology Reports

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Tanshinone IIA (TSN) exhibits a variety of anticancer effects. However, whether it inhibits gastric cancer (GC) cell proliferation and migration and the mechanism remain unclear. In the present study, different concentrations of TSN were co-incubated with SGC-7901 cells. The pcDNA-FOXM1 or FOXM1-siRNA plasmid was transfected into cells before treatment with 5 µg/l TSN. The proliferation and migration abilities of the SGC-7901 cells were tested by MTT and wound healing assays. Western blotting was used to investigate the expression levels of P21, Ki-67, PCNA, MMP-2, MMP-9 and FOXM1. We found that compared with the control, the proliferation and migration abilities of the SGC-7901 cells were decreased after incubation with different concentrations of TSN in a dose-dependent manner (p<0.01). Moreover, the expression levels of Ki-67, PCAN, MMP-2, MMP-9 and FOXM1 were decreased, and P21 was increased in the TSN-treated SGC-7901 cells (p<0.01). In addition, downregulation of FOXM1 by FOXM1-siRNA had the same effect as TSN on SGC-7901 cells, and overexpression of FOXM1 partly abrogated TSN-mediated inhibition of SGC-7901 cell proliferation and migration. These results suggested that TSN inhibits SGC-7901 cell proliferation and migration by downregulation of FOXM1.

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

Cited by 35 publications

References 29 publications

PLK1, A Potential Target for Cancer Therapy

PLK1, A Potential Target for Cancer Therapy

FOXK2 suppresses the malignant phenotype and induces apoptosis through inhibition of EGFR in clear‐cell renal cell carcinoma

Tanshinone IIA suppresses gastric cancer cell proliferation and migration by downregulation of FOXM1

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