FOXO1 is a tumor suppressor in cervical cancer

Zhang, B; Gui, Linsheng; Zhao, Xiao-Lian; Zhu, Lifei; Li, Q W

doi:10.4238/2015.june.18.3

Cited by 57 publications

(55 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We first examined the expression level of the transcriptional factor, FOXO1, in four different cervical cancer cell lines (HeLa, Caski, SiHa, and C-33A). Our results confirmed that two well-characterized cell lines, C-33A and Siha expressed FOXO1 at the highest and lowest levels, respectively (Zhang et al, 2015).…”

Section: Discussionsupporting

confidence: 83%

Forkhead box protein O1 mediates apoptosis in a cancer cervical cell line treated with the antitumor agent tumor necrosis factor-α

Zhang¹,

Gui²,

Zhu³

et al. 2015

Genet. Mol. Res.

Self Cite

View full text Add to dashboard Cite

ABSTRACT. Tumor necrosis factor-α (TNF-α) is an important proapoptotic cytokine, which performs a broad range of immune and inflammatory functions in several vital processes. TNF-α-induced apoptosis has been confirmed, however, relatively little is known regarding the role of forkhead box class-O 1 (FOXO1) in mediating TNF-α-induced apoptosis in cervical cancer. In our study, we used the well-characterized cervical cancer cell line C-33A to investigate the role of FOXO1. The results showed that the antitumor agent TNF-α increased the expression level of FOXO1 (P < 0.05) and enhanced its transcriptional activity (P < 0.05). Furthermore, knockdown of FOXO1 repressed TNF-α-induced apoptosis and caspase-3, 8, and 9 expressions (P < 0.05). Collectively, these findings suggest that TNF-α upregulated the transcriptional factor FOXO1, leading to an increased expression of apoptotic gene, which leads to an increase in apoptosis.

show abstract

Section: Discussionsupporting

confidence: 83%

Forkhead box protein O1 mediates apoptosis in a cancer cervical cell line treated with the antitumor agent tumor necrosis factor-α

Zhang¹,

Gui²,

Zhu³

et al. 2015

Genet. Mol. Res.

Self Cite

View full text Add to dashboard Cite

show abstract

“…Research shows the vital involvement of FOX family in cancer onset and progression, and miRNAs play a crucial regulatory role in tumors via the modulation of these FOX proteins (Zhang et al, 2015;Wang et al, 2016). Foxf2 gene belongs to the forkhead/winged helix transcription factor family and has been implicated as an oncogene that modulates metastasis of various tumors (Nilsson et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

Research Article MiR-200c inhibits metastasis of breast tumor via the downregulation of Foxf2.

et al. 2017

View full text Add to dashboard Cite

ABSTRACT. The forkhead box F2 (Foxf2) gene suppresses epithelial-mesenchymal transition via the modulation of transcription of zinc finger E-box-binding homeobox 1 (Zeb1) and epithelial (E)-cadherin, thereby inhibiting tumor metastasis. Additionally, the specific binding of microRNA (miR)-200c to Foxf2 mRNA impedes metastatic pulmonary cancer. However, the role of miR-200c in breast cancer is still unknown. Therefore, in this study, miR-200c mimics were transfected into the highly metastatic breast cancer cell line MDA-MB-231. Their invasion and migration abilities were observed by scratch and transwell migration assays. Real-time PCR was used to detect mRNA levels of Foxf2, Zeb1, and E-cadherin, whereas Foxf2 protein level was determined by western blot analysis. Our results showed that, compared to the control group, miR-200c inhibited the migration or invasion of MDA-MB-231 cells. Real-time PCR and western blot analysis exhibited significant decreases in Foxf2 expression in the presence of miR-200c, along with a decrease in Zeb1 and increase in E-cadherin mRNA expressions. Thus, our preliminary data demonstrated that miR-200c could inhibit the metastasis of breast cancer cells by downregulating Foxf2 expression, providing leads for the discovery of a novel breast cancer treatment.

show abstract

“…When FOXO1 is overexpressed, cell proliferation and growth is inhibited by upregulating caspase-3 and caspase-9 and inducing G2/M arrest and (Yang et al 2015). BCL2L1 and BCL2L2, BCL2 family, are pro-oncogene and repress intrinsic pathwaymediated cell death (Denoyelle et al 2014;Zhang et al 2015). Other genes, PTEN, BBC3, and MDM2, also rescue cell death and induce proliferation (Fortunato et al 2014;Zhang et al 2010).…”

Section: Discussionmentioning

confidence: 99%

Epigallocatechin-3-gallate inhibits paclitaxel-induced apoptosis through the alteration of microRNA expression in human dermal papilla cells

Shin

Jun

Kim³

et al. 2018

biomed dermatol

View full text Add to dashboard Cite

Background: Paclitaxel well known as anti-cancer drug has been shown to cause alopecia in chemotherapy. The paclitaxel chemotherapy-mediated alopecia is induced by apoptotic damage in human dermal papilla (HDP) cells. Epigallocatechin-3-gallate (EGCG) inhibits apoptosis against anti-cancer drug such as cisplatin. EGCG, one of the green tea extract ingredients, has been reported to enhance cell viability and to inhibit apoptosis. However, it is unclear that EGCG enhances cell viability and inhibits apoptosis against paclitaxel-induced apoptotic damage in HDP cells. Methods: We show cell viability, cell cycle, and microRNA (miRNA) expression in EGCG-mediated rescue cell to paclitaxel-mediated cell death and growth arrest. Results: EGCG promotes cell survival and cell death inhibitory effects and alteration of miRNA expression in paclitaxelexposed HDP cells were investigated. Firstly, paclitaxel increases apoptosis and EGCG promotes cell survival and represses paclitaxel-induced apoptosis in a dose-dependent manner. Fluorescence-activated cell sorting (FACS) analysis showed that EGCG protects apoptosis in paclitaxel-exposed HDP cells. miRNA microarray analysis was performed and 48 miRNAs changed by EGCG in paclitaxel-exposed HDP cells were identified. In gene ontology analysis in silico, miRNAs regulate apoptosis and cell proliferation-regulated genes, such as BCL2L1, BCL2L2, BBC3, and MDM2. In Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, miRNAs are related to mitogen-activated protein kinase (MAPK) signaling pathway and Wnt signaling pathway, which regulate apoptosis and cell proliferation. Conclusions: EGCG inhibits apoptosis through regulating miRNA expression related to apoptosis and cell proliferation in paclitaxel-treated HDP cells.

show abstract

FOXO1 is a tumor suppressor in cervical cancer

Cited by 57 publications

References 28 publications

Forkhead box protein O1 mediates apoptosis in a cancer cervical cell line treated with the antitumor agent tumor necrosis factor-α

Forkhead box protein O1 mediates apoptosis in a cancer cervical cell line treated with the antitumor agent tumor necrosis factor-α

Research Article MiR-200c inhibits metastasis of breast tumor via the downregulation of Foxf2.

Epigallocatechin-3-gallate inhibits paclitaxel-induced apoptosis through the alteration of microRNA expression in human dermal papilla cells

Contact Info

Product

Resources

About