scholarly journals FOXO4 overexpression suppresses hypoxia-induced-MCF-7 cell survival and promotes apoptosis through the HIF-2α/Bnip3 signal pathway

RSC Advances ◽  
2019 ◽  
Vol 9 (44) ◽  
pp. 25912-25918
Author(s):  
Yan Qiao ◽  
Bin Wang ◽  
Huimin Zhang ◽  
Yu Yan ◽  
Ligang Niu
Keyword(s):  
Cell Survival ◽  
Transcriptional Regulator ◽  
Signal Pathway ◽  
Tumour Suppressor ◽  
Forkhead Box ◽  
Mcf 7

Transcriptional regulator forkhead box O (FOXO) has implications in many diverse carcinomas and often acts as a tumour suppressor.

scholarly journals Retraction: FOXO4 overexpression suppresses hypoxia-induced-MCF-7 cell survival and promotes apoptosis through the HIF-2α/Bnip3 signal pathway

RSC Advances ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 4573-4573
Author(s):  
Laura Fisher
Keyword(s):  
Cell Survival ◽  
Signal Pathway ◽  
Mcf 7

Retraction of ‘FOXO4 overexpression suppresses hypoxia induced-MCF-7 cell survival and promotes apoptosis through HIF-2α/Bnip3 signal pathway’ by Yan Qiao et al., RSC Adv., 2019, 9, 25912–25918, DOI: 10.1039/C9RA04380B.

scholarly journals FOXC1 in cancer development and therapy: deciphering its emerging and divergent roles

2017 ◽  
Vol 9 (12) ◽  
pp. 797-816 ◽  
Author(s):  
Zhi Yang ◽  
Shuai Jiang ◽  
Yicheng Cheng ◽  
Tian Li ◽  
Wei Hu ◽  
...  
Keyword(s):  
Transcriptional Regulator ◽  
Cancer Development ◽  
Protein Activity ◽  
Stem Cell Maintenance ◽  
Cancer Migration ◽  
Forkhead Box ◽  
Pathological Conditions ◽  
Clinical Biomarker ◽  
Abnormal Cell Proliferation ◽  
Cell Maintenance

Forkhead box C1 (FOXC1) is an essential member of the forkhead box transcription factors and has been highlighted as an important transcriptional regulator of crucial proteins associated with a wide variety of carcinomas. FOXC1 regulates tumor-associated genes and is regulated by multiple pathways that control its mRNA expression and protein activity. Aberrant FOXC1 expression is involved in diverse tumorigenic processes, such as abnormal cell proliferation, cancer stem cell maintenance, cancer migration, and angiogenesis. Herein, we review the correlation between the expression of FOXC1 and tumor behaviors. We also summarize the mechanisms of the regulation of FOXC1 expression and activity in physiological and pathological conditions. In particular, we focus on the pathological processes of cancer targeted by FOXC1 and discuss whether FOXC1 is good or detrimental during tumor progression. Moreover, FOXC1 is highlighted as a clinical biomarker for diagnosis or prognosis in various human cancers. The information reviewed here should assist in experimental designs and emphasize the potential of FOXC1 as a therapeutic target for cancer.

scholarly journals SGK3 Is an Estrogen-Inducible Kinase Promoting Estrogen-Mediated Survival of Breast Cancer Cells

2011 ◽  
Vol 25 (1) ◽  
pp. 72-82 ◽  
Author(s):  
Yuanzhong Wang ◽  
Dujin Zhou ◽  
Sheryl Phung ◽  
Selma Masri ◽  
David Smith ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Protein Kinase ◽  
Cell Survival ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Dependent Manner ◽  
Binding Regions ◽  
Er Positive ◽  
Mcf 7 ◽  
Positive Breast Cancer

Serum- and glucocorticoid-inducible kinase 3 (SGK3) is a protein kinase of the AGC family of protein kinase A, protein kinase G, and protein kinase C and functions downstream of phosphatidylinositol 3-kinase (PI3K). Recent study revealed that SGK3 plays a pivotal role in Akt/protein kinase B independent signaling downstream of oncogenic PI3KCA mutations in breast cancer. Here we report that SGK3 is an estrogen receptor (ER) transcriptional target and promotes estrogen-mediated cell survival of ER-positive breast cancer cells. Through a meta-analysis on 22 microarray studies of breast cancer in the Oncomine database, we found that the expression of SGK3 is significantly higher (5.7-fold, P < 0.001) in ER-positive tumors than in ER-negative tumors. In ER-positive breast cancer cells, SGK3 expression was found to be induced by 17β-estradiol (E2) in a dose- and time-dependent manner, and the induction of SGK3 mRNA by E2 is independent of newly synthesized proteins. We identified two ERα-binding regions at the sgk3 locus through chromatin immunoprecipitation with massively parallel DNA sequencing. Promoter analysis revealed that ERα stimulates the activity of sgk3 promoters by interaction with these two ERα-binding regions on E2 treatment. Loss-of-function analysis indicated that SGK3 is required for E2-mediated cell survival of MCF-7 breast carcinoma cells. Moreover, overexpression of SGK3 could partially protect MCF-7 cells against apoptosis caused by antiestrogen ICI 182,780. Together, our study defines the molecular mechanism of regulation of SGK3 by estrogen/ER and provides a new link between the PI3K pathway and ER signaling as well as a new estrogen-mediated cell survival mechanism mediated by SGK3 in breast cancer cells.

miR-938 Promotes the Proliferation and Invasion of Prostate Cancer Through Targeting Pleckstrin Homology (PH) Domain Leucine-Rich-Repeats Protein Phosphatase 2 and Forkhead Box O3

2019 ◽  
Vol 9 (5) ◽  
pp. 583-591
Author(s):  
Xin Deng ◽  
Fengye Wang ◽  
Qianjin Zhang ◽  
Xuejian Yang ◽  
Hao Liu ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Protein Phosphatase ◽  
Mrna Level ◽  
Signal Pathway ◽  
Migration And Invasion ◽  
Ph Domain ◽  
Pleckstrin Homology ◽  
Forkhead Box ◽  
Protein Phosphatase 2 ◽  
Leucine Rich Repeats

miR-938 is generally reported to be up-regulated in various cancers, which affect the tumor progression. In the present study, we investigated the biological role and underlying mechanisms of miR-938 in prostate cancer (PCa). PCa is the most common malignant tumor in males with markedly increasing incidence in recent years. Up-regulation of miR-938 occurred in PCa tissues and cell lines at mRNA level. Functional assays were established to demonstrate that miR-938 mimics significantly promoted the proliferation, migration and invasion of PCa cells, while knockdown of miR-938 led to the inhibition. Luciferase activity assay suggested miR-938 directly bound to the 3 UTR of PHLPP2 (Pleckstrin Homology (PH) domain Leucine-rich-repeats Protein Phosphatase 2) and FOXO3 (Forkhead box O3). Our results also showed that the regulation activity of miR-938 on progression of PCa was partially through its negative regulation on PHLPP2 and FOXO3. Our results deciphered the mechanism through which miR-938 promoted the progression of PCa by activation of PI3K/AKT signal pathway. Together, inactivation of PI3K/AKT signal pathway through down-regulation of miR-938 could be an important mechanism in inhibiting PCa progression, thus shedding light on the development of novel anti-tumor therapies for treatment of PCa.

Regulation of cell survival and proliferation by the FOXO (Forkhead box, class O) subfamily of Forkhead transcription factors

2003 ◽  
Vol 31 (1) ◽  
pp. 292-297 ◽  
Author(s):  
K.U. Birkenkamp ◽  
P.J. Coffer
Keyword(s):  
Transcription Factors ◽  
Cell Survival ◽  
Cell Fate ◽  
Nuclear Export ◽  
Molecular Mechanisms ◽  
Target Genes ◽  
Acute Lymphocytic Leukaemia ◽  
Cell Fate Decisions ◽  
Forkhead Transcription Factors ◽  
Forkhead Box

Recently, the FOXO (Forkhead box, class O) subfamily of Forkhead transcription factors has been identified as direct targets of phosphoinositide 3-kinase-mediated signal transduction. The AFX (acute-lymphocytic-leukaemia-1 fused gene from chromosome X), FKHR (Forkhead in rhabdomyosarcoma) and FKHR-L1 (FKHR-like 1) transcription factors are directly phosphorylated by protein kinase B, resulting in nuclear export and inhibition of transcription. This signalling pathway was first identified in the nematode worm Caenorhabditis elegans, where it has a role in regulation of the life span of the organism. Studies have shown that this evolutionarily conserved signalling module has a role in regulation of both cell-cycle progression and cell survival in higher eukaryotes. These effects are co-ordinated by FOXO-mediated induction of a variety of specific target genes that are only now beginning to be identified. Interestingly, FOXO transcription factors appear to be able to regulate transcription through both DNA-binding-dependent and -independent mechanisms. Our understanding of the regulation of FOXO activity, and defining specific transcriptional targets, may provide clues to the molecular mechanisms controlling cell fate decisions to divide, differentiate or die.

Expression of Phosphatase and Tensin Homolog Deleted on Chromosome Ten on the Development of Cisplatin Resistance in Breast Cancer by TGF-β1 Signal Pathway

2021 ◽  
Vol 11 (10) ◽  
pp. 1900-1907
Author(s):  
Yuan-Ding Zhang ◽  
Zhen-Xia Wang ◽  
Yan Zhang ◽  
Jin Pei
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Cisplatin Resistance ◽  
Signal Pathway ◽  
Lymph Node Status ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Mcf 7

Introduction: This study aims to evaluate the expression of PTEN on the development of cisplatin resistance in breast cancer by TGF-β1 signal pathway in order to investigate the prognostic value of PTEN and TGF-β1 for breast cancer. Material and Methods: In this study, HE staining, Immunohistochemical staining, Immunofluorescence and Western blotting were used to detect the expression of PTEN and TGF-β1 in breast cancer MCF-7 cells to explain clearly the relationship between PTEN and TGF-β1 on TGF-β1 treated MCF-7 Cells. Results: The experiment results showed the expression of PTEN and TGF-β1 in Human breast cancer increased obviously compared with paracancerous tissues (P < 0.05). The expression of PTEN and TGF-β1 was closely correlated with tumor size, distant metastasis, pathological stage and progesterone receptor status, but not with age and lymph node status. At the same time, the expression of PTEN and TGF-β1 in cisplatin-treated MCF-7 Cells reduced as compared with untreated breast cancer cells (P < 0.05). In addition, the expression of PTEN increased by TGF-β1 inducer treated Human Breast Cancer Cells. However, the expression of PTEN in TGF-β1 inhibitor treated Human Breast Cancer Cells was lower than in untreated breast cancer cells (P < 0.05). Conclusions: PTEN and TGF-β1 played an important role in Human Breast cancer. In addition, the expression of PTEN could be regulated by TGF-β1 in Cisplatin and TGF-β1 treated Human Breast Cancer Cells.

Ascorbic acid and cell survival of adriamycin resistant and sensitive MCF-7 breast tumor cells

1995 ◽  
Vol 18 (4) ◽  
pp. 699-708 ◽  
Author(s):  
William W. Wells ◽  
Pamela A. Rocque ◽  
Dian-Peng Xu ◽  
Elizabeta B. Meyer ◽  
Leigh J. Charamella ◽  
...  
Keyword(s):  
Ascorbic Acid ◽  
Cell Survival ◽  
Tumor Cells ◽  
Breast Tumor ◽  
Breast Tumor Cells ◽  
Mcf 7
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