FOXQ1 is overexpressed in laryngeal carcinoma and affects cell growth, cell cycle progression and cell invasion

Zhang, Jie; Li, Wei; Song, Dae‐Kyu; Tai, Xuhui; Jia, Jianping; Guo, Xing

doi:10.3892/ol.2015.3530

Cited by 11 publications

(9 citation statements)

References 29 publications

(29 reference statements)

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“…Moreover, FOXQ1 has a significant function in tumor growth in bladder cancer (22). FOXQ1 promotes the invasive ability of laryngeal carcinoma (23) and enhances the metastasis of hepatocellular carcinoma and non-small cell lung cancer by regulating EMT (4,17). However, the role of FOXQ1 in prostate cancer remains poorly understood.…”

Section: Inhibition Of Foxq1 Induces Apoptosis and Suppresses Prolifementioning

confidence: 99%

Inhibition of FOXQ1 induces apoptosis and suppresses proliferation in prostate cancer cells by controlling BCL11A/MDM2 expression

Zhang

Wang

et al. 2016

Oncology Reports

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Forkhead box Q1 (FOXQ1) has been recognized as an oncogene that is overexpressed in different cancers, and several studies have shown that FOXQ1 is related to apoptosis and proliferation in many cancer types. However, the role and the molecular mechanism of FOXQ1 in prostate cancer remains unclear. In this study, we aimed to explore the role of FOXQ1 in regulating cell apoptosis, proliferation and invasion in prostate cancer and the underlying mechanism. We found that FOXQ1 was highly expressed in the prostate cancer tissues and cell lines. In our FOXQ1 loss-of-function experiments, the data indicate that the expression of BCL11A and MDM2 was significantly downregulated, prostate cancer cell proliferation and invasion were markedly suppressed, and apoptosis was significantly induced. Moreover, overexpression of BCL11A obviously reversed the effect of FOXQ1 inhibition on apoptosis, proliferation and invasion of prostate cancer cells. In addition, BCL11A overexpression also abrogated the inhibitory effect of FOXQ1 suppression on MDM2 expression. Taken together, our study suggests that FOXQ1 regulates prostate cancer cell proliferation and apoptosis by regulating BCL11A/MDM2 expression and indicates that FOXQ1 may serve as a potential therapeutic target for prostate cancer.

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Section: Inhibition Of Foxq1 Induces Apoptosis and Suppresses Prolifementioning

confidence: 99%

Inhibition of FOXQ1 induces apoptosis and suppresses proliferation in prostate cancer cells by controlling BCL11A/MDM2 expression

Zhang

Wang

et al. 2016

Oncology Reports

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show abstract

“…The FoxQ1 is an evolutionarily conserved protein with 100% amino acid sequence similarity in the DNA binding domain between human, mouse, and rat 20,21 . Overexpression of protein or mRNA levels of FoxQ1 has been reported in different cancers, including gastric cancer, hepatocellular carcinoma, laryngeal carcinoma, pancreatic cancer, colorectal cancer, and breast cancer 8,10,22‐27 . We showed previously that the level of FoxQ1 protein is higher by 18.4‐fold in basal‐like human breast cancers compared with normal mammary tissue 10 .…”

Section: Discussionmentioning

confidence: 98%

“…To the contrary, overexpression of FoxQ1 in non–small‐cell lung cancer cell lines (A549 and HCC827) results in increased proliferation when compared with corresponding EV cells 34 . Cell proliferation is decreased upon FoxQ1 knockdown in a laryngeal carcinoma cell line 24 . Because the full spectrum of the FoxQ1‐regulated transcriptome is still not fully appreciated, further work may shed light as to why FoxQ1 overexpression is unable to increase breast cancer cell proliferation.…”

Section: Discussionmentioning

confidence: 99%

Novel mechanistic targets of forkhead box Q1 transcription factor in human breast cancer cells

Kim

Hahm

Singh

et al. 2020

Molecular Carcinogenesis

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The transcription factor forkhead box Q1 (FoxQ1) is overexpressed in different solid tumors including breast cancer, but the mechanism underlying its oncogenic function is still not fully understood. In this study, we compared RNA‐seq data from FoxQ1 overexpressing SUM159 cells with that of empty vector‐transfected control cells to identify novel mechanistic targets of this transcription factor. Analysis of The Cancer Genome Atlas (TCGA) data set revealed significantly higher expression of FoxQ1 in black breast cancer patients compared with white women with this disease. In contrast, expression of FoxQ1 was comparable in ductal and lobular carcinomas in the breast cancer TCGA data set. Complementing our published findings in basal‐like subtype, immunohistochemistry revealed upregulation of FoxQ1 protein in luminal‐type human breast cancer tissue microarrays when compared with normal mammary tissues. Many previously reported transcriptional targets of FoxQ1 (eg, E‐cadherin, N‐cadherin, fibronectin 1, etc) were verified from the RNA‐seq analysis. FoxQ1 overexpression resulted in the downregulation of genes associated with cell cycle checkpoints, M phase, and cellular response to stress/external stimuli as evidenced from the Reactome pathway analysis. Consequently, FoxQ1 overexpression resulted in mitotic arrest in basal‐like SUM159 and human mammary epithelial cell line, but not in luminal‐type MCF‐7 cells. Finally, we show for the first time that FoxQ1 is a direct transcriptional regulator of interleukin (IL)‐1α, IL‐8, and vascular endothelial growth factor in breast cancer cells as evidenced by chromatin immunoprecipitation assay. In conclusion, the present study reports novel mechanistic targets of FoxQ1 in human breast cancer cells.

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“…To the contrary, overexpression of FoxQ1 in non-small cell lung cancer cell lines (A549 and HCC827) results in increased proliferation when compared to corresponding EV cells (31). Cell proliferation is decreased upon FoxQ1 knockdown in a laryngeal carcinoma cell line (21). Because the full spectrum of the FoxQ1-regulated transcriptome is still not fully appreciated, further work may shed light as to why FoxQ1 overexpression is unable to increase breast cancer cell proliferation.…”

Section: Discussionmentioning

confidence: 99%

“…The FoxQ1 is an evolutionary conserved protein with 100% amino acid sequence similarity in the DNA binding domain between human, mouse, and rat (17,18). Overexpression of protein or mRNA levels of FoxQ1 has been reported in different cancers, including gastric cancer, hepatocellular carcinoma, laryngeal carcinoma, pancreatic cancer, colorectal cancer, and breast cancer (8,10,(19)(20)(21)(22)(23)(24). We showed previously that the level of FoxQ1 protein is higher by 18.4-fold in basal-like human breast cancers compared to normal mammary tissue (10).…”

Section: Discussionmentioning

confidence: 99%

Novel mechanistic targets of Forkhead box Q1 transcription factor in human breast cancer cells

Kim

Hahm

Singh

et al. 2020

Preprint

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The transcription factor forkhead box Q1 (FoxQ1), which is overexpressed in different solid tumors, has emerged as a key player in the pathogenesis of breast cancer by regulating epithelialmesenchymal transition, maintenance of cancer-stem like cells, and metastasis. However, the mechanism underlying oncogenic function of FoxQ1 is still not fully understood. In this study, we compared the RNA-seq data from FoxQ1 overexpressing SUM159 cells with that of empty vector-transfected control (EV) cells to identify novel mechanistic targets of this transcription factor. Consistent with published results in basal-like subtype, immunohistochemistry revealed upregulation of FoxQ1 protein in luminal-type human breast cancer tissue microarrays when compared to normal mammary tissues. Many previously reported transcriptional targets of FoxQ1 (e.g., E-cadherin, N-cadherin, fibronectin 1, etc.) were verified from the RNA-Seq analysis. FoxQ1 overexpression resulted in downregulation of genes associated with cell cycle checkpoints, M phase, and cellular response to stress/external stimuli as evidenced from the Reactome pathway analysis.Consequently, FoxQ1 overexpression resulted in S, G2M and mitotic arrest in basal-like SUM159 and HMLE cells, but not in luminal-type MCF-7 cells. There were differences in expression of cell cycle-associated proteins between FoxQ1 overexpressing SUM159 and MCF-7 cells. Finally, we show for the first time that FoxQ1 is a direct transcriptional regulator of interleukin (IL)-1α, IL-8, and vascular endothelial growth factor in breast cancer cells. Chromatin immunoprecipitation revealed FoxQ1 occupancy at the promoters of IL-1α, IL-8, and VEGF. In conclusion, the present study reports novel mechanistic targets of FoxQ1 in human breast cancer cells.

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FOXQ1 is overexpressed in laryngeal carcinoma and affects cell growth, cell cycle progression and cell invasion

Cited by 11 publications

References 29 publications

Inhibition of FOXQ1 induces apoptosis and suppresses proliferation in prostate cancer cells by controlling BCL11A/MDM2 expression

Inhibition of FOXQ1 induces apoptosis and suppresses proliferation in prostate cancer cells by controlling BCL11A/MDM2 expression

Novel mechanistic targets of forkhead box Q1 transcription factor in human breast cancer cells

Novel mechanistic targets of Forkhead box Q1 transcription factor in human breast cancer cells

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