FOXC2 positively regulates YAP signaling and promotes the glycolysis of nasopharyngeal carcinoma

Song, Lijuan; Tang, Huiping; Liao, Wenjing; Luo, Xinggu; Li, Yanmei; Chen, Tao; Zhang, Xiaowen

doi:10.1016/j.yexcr.2017.04.019

Cited by 34 publications

(22 citation statements)

References 16 publications

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“…2e, Song et al found that YAP is positively regulated by forkhead box protein C2 (FOXC2). Activation of YAP specifically elevates the expression of Hexokinase 2 (HK2) at both mRNA and protein level [36]. Functionally, FOXC2 acts as a bridge to interact with YAP and TEAD, and forms a FOXC2-YAP-TEAD complex, which leading to activation of HK2 and eventually promote glycolysis in nasopharyngeal carcinoma cells [36].…”

Section: Main Textmentioning

confidence: 99%

“…Activation of YAP specifically elevates the expression of Hexokinase 2 (HK2) at both mRNA and protein level [36]. Functionally, FOXC2 acts as a bridge to interact with YAP and TEAD, and forms a FOXC2-YAP-TEAD complex, which leading to activation of HK2 and eventually promote glycolysis in nasopharyngeal carcinoma cells [36]. However, the FOXC2-YAP-TEAD complex does not bind to the promoter region of HK2, even though this complex has a positive effect on the HK2 transcriptional regulation.…”

Section: Main Textmentioning

confidence: 99%

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The role of YAP/TAZ activity in cancer metabolic reprogramming

et al. 2018

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In contrast to normal cells, which use the aerobic oxidation of glucose as their main energy production method, cancer cells prefer to use anaerobic glycolysis to maintain their growth and survival, even under normoxic conditions. Such tumor cell metabolic reprogramming is regulated by factors such as hypoxia and the tumor microenvironment. In addition, dysregulation of certain signaling pathways also contributes to cancer metabolic reprogramming. Among them, the Hippo signaling pathway is a highly conserved tumor suppressor pathway. The core oncosuppressive kinase cascade of Hippo pathway inhibits the nuclear transcriptional co-activators YAP and TAZ, which are the downstream effectors of Hippo pathway and oncogenic factors in many solid cancers. YAP/TAZ function as key nodes of multiple signaling pathways and play multiple regulatory roles in cancer cells. However, their roles in cancer metabolic reprograming are less clear. In the present review, we examine progress in research into the regulatory mechanisms of YAP/TAZ on glucose metabolism, fatty acid metabolism, mevalonate metabolism, and glutamine metabolism in cancer cells. Determining the roles of YAP/TAZ in tumor energy metabolism, particularly in relation to the tumor microenvironment, will provide new strategies and targets for the selective therapy of metabolism-related cancers.

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Section: Main Textmentioning

confidence: 99%

Section: Main Textmentioning

confidence: 99%

The role of YAP/TAZ activity in cancer metabolic reprogramming

et al. 2018

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“…Indeed, FOXC2 overexpression and nuclear localization are poor prognostic indicators of survival in patients with prostate cancer (2), hepatocellular carcinoma (3), NSCLC (4), colorectal cancer (5), glioma (6), gastric cancer (7), and esophageal as well as oral tongue squamous cell carcinomas (8,9). Studies employing murine and human tumor cell lines have confirmed the oncogenic potential of the FOXC2 transcription factor, highlighting its ability to promote several hallmarks of cancer progression, including proliferation (5,9), epithelial-mesenchymal transition (EMT) (10), invasion and metastasis (11), glycolytic metabolism (12), stemness (13), and drug resistance (14,15). Based on these diverse tumor-promoting functions and the breadth of tumor types in which FOXC2 is dysregulated, it is important to improve our understanding of this transcription factor's regulation of oncogenic pathways in cancer cells.…”

Section: Introductionmentioning

confidence: 99%

RNA-seq Analysis of Wild-Type vs. FOXC2-Deficient Melanoma Cells Reveals a Role for the FOXC2 Transcription Factor in the Regulation of Multiple Oncogenic Pathways

Hargadon

Williams

2020

Front. Oncol.

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“…FOXC2 was identified to induce epithelial-mesenchymal transition (EMT) in prostate cancer [9],lung cancer [10]. Overexpression of FOXC2 was related to poor prognosis of hepatocellular carcinoma [11].FOXC2 activated YAP signal pathway and enhanced the glycolysis in nasopharyngeal carcinoma cells [12]. Still FOXC2 was certificated to promote EMT, migration and invasion in cisplatin-resistant ovarian cancer cells [13].…”

Section: Introductionmentioning

confidence: 99%

Functional polymorphisms in FOXC2 gene and Epithelial ovarian Cancer susceptibility in Chinese population

Zhou

Zou

et al. 2020

J Ovarian Res

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Background: Epithelial ovarian cancer (EOC) is highly lethal gynecological cancer. Forkhead Box Protein C2 (FOXC2) promotes occurrence and development of various malignant tumors. The present study is aimed at exploring the correlation between the polymorphism of FOXC2 and epithelial ovarian cancer susceptibility in Chinese Han population. Methods: A case-control design was used to verify the association between FOXC2 polymorphisms and epithelial ovarian cancer. The genotyping was performed using Taqman® SNP Genotyping kit by qRT-PCR. The genetic variants including rs3751794 C > T, rs1035550 A > G, rs4843163 C > G and rs4843396 C > T in FOXC2 gene were analyzed. The strength of the associations was detected using odds ratios and 95% confidence intervals. Stratification analyses showed the association between the FOXC2 gene polymorphisms rs3751794 C > T, rs4843163 C > G and rs4843396 C > T with epithelial ovarian cancer susceptibility in terms of age, metastasis status, clinical stage, pathological grade, pregnant times, pausimenia, and the expression of ER, PR, wild p53 and mutant p53. Results: Rs3751794 C > T (P = 0.0016), rs4843163 C > G (P < 0.0001) and rs4843396 C > T (P < 0.0001) were significantly associated with increased epithelial ovarian cancer risk. In stratification analyses,rs3751794 C > T, was identified to be dominant in no metastasis patients, clinical stage 4 group, middle grade pathological stage, pregnant time over 3 patients, post-menopause women, strong wild type p53 expression; rs4843163 C > G was dominant in high grade clinical stage, high grade pathological stage, post-menopause women, strong ER expression group and no mutant p53 expression group; rs4843396 C > T was dominant in high grade clinical stage, high grade pathological stage, strong ER expression group. The rs1035550 A > G was not related to epithelial ovarian cancer susceptibility. Conclusions:The results of the current study verified that FOXC2 gene polymorphisms were associated with increased epithelial ovarian cancer risk and suggested that FOXC2 gene polymorphisms might be a potential biomarker for epithelial ovarian cancer susceptibility.

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FOXC2 positively regulates YAP signaling and promotes the glycolysis of nasopharyngeal carcinoma

Cited by 34 publications

References 16 publications

The role of YAP/TAZ activity in cancer metabolic reprogramming

The role of YAP/TAZ activity in cancer metabolic reprogramming

RNA-seq Analysis of Wild-Type vs. FOXC2-Deficient Melanoma Cells Reveals a Role for the FOXC2 Transcription Factor in the Regulation of Multiple Oncogenic Pathways

Functional polymorphisms in FOXC2 gene and Epithelial ovarian Cancer susceptibility in Chinese population

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