β-Catenin/Tcf7l2–dependent transcriptional regulation of GLUT1 gene expression by Zic family proteins in colon cancer

Zhao, Zibo; Wang, Lu; Bartom, Elizabeth T.; Marshall, Stacy A.; Rendleman, Emily J.; Ryan, Caila; Shilati, Anthony; Savas, Jeffrey N.; Chandel, Navdeep S.; Shilatifard, Ali

doi:10.1126/sciadv.aax0698

Cited by 35 publications

(39 citation statements)

References 60 publications

(70 reference statements)

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“…Further, the present study revealed that the silencing of β‐catenin could reverse the upregulation of GLUT1 caused by the silencing HDAC4. It has also been previously suggested that the Wnt/β‐catenin pathway exerts its effects on colorectal cancer cells through mediating GLUT1 33 . GLUT1 has been highlighted to be a downstream glycolytic target gene of β‐catenin signaling, and they share a positive correlation in expression 34 .…”

Section: Discussionmentioning

confidence: 98%

“…It has also been previously suggested that the Wnt/β-catenin pathway exerts its effects on colorectal cancer cells through mediating GLUT1. 33 GLUT1 has been highlighted to be a downstream glycolytic target gene of β-catenin signaling, and they share a positive correlation in expression. 34 Moreover, inhibition of TUG1 was found to competitively bind to miR-145-5p to target Bnip3 and inactivate the Wnt/β-catenin signaling pathway, hence alleviating the myocardial cell injury induced by hypoxia.…”

Section: Discussionmentioning

confidence: 99%

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LncRNA TUG1 competitively binds to miR‐340 to accelerate myocardial ischemia‐reperfusion injury

Liu

et al. 2020

FASEB j.

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The aberrant expression of long noncoding RNA (lncRNA) taurine-upregulated gene 1 (TUG1) has been previously associated with myocardial ischemia-reperfusion injury (MIRI), but the underlying molecular mechanisms remain elusive. The current study aimed to clarify the functional role of TUG1/microRNA (miR)-340/histone deacetylase 4 (HDAC4)/β-catenin/glucose transporter type 1 (GLUT1) axes in MIRI. The database-based analyses performed predicted the downstream factors of lncRNA TUG1. In the MIRI mouse models and hypoxia/reoxygenation (H/R)-induced cardiomyocyte models, the expression of TUG1/miR-340/HDAC4/β-catenin/GLUT1 was manipulated to examine their effects on the infarction area, cardiomyocyte viability and apoptosis employing the Evans blue/TTC double staining, CCK-8 and TUNEL assays. Furthermore, the dual luciferase reporter and RIP assays verified the binding affinity of miR-340 to TUG1 and HDAC4. Subsequently, a negative correlation between miR-340 and TUG1 or HDAC4 expression was identified in myocardial tissues of MIRI mice and H/R-induced cardiomyocyte models, along with a positive correlation between TUG1 and HDAC4. Additionally, it was established that TUG1 bound to miR-340, and miR-340 targeted HDAC4. TUG1 upregulated HDAC4 expression, thereby promoting MIRI in the mouse models. HDAC4 was proven to repress the expression of β-catenin and its target gene GLUT1. Moreover, the in vivo experiments validated that the inhibition of TUG1/miR-340/HDAC4/β-catenin/ GLUT1 axes alleviated MIRI in mice. Collectively, the current study uncovered the role of TUG1/miR-340/HDAC4/β-catenin/GLUT1 axes in MIRI mouse models and H/R-induced cardiomyocyte models which may be a potential therapeutic target for MIRI treatment.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

LncRNA TUG1 competitively binds to miR‐340 to accelerate myocardial ischemia‐reperfusion injury

Liu

et al. 2020

FASEB j.

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“…38 A recent study revealed that Zic5 could suppress the transcription of GLUT1 in a β-catenin/TCF4-dependent manner to downregulate glucose uptake in HCT116 colon cancer cells, while Zic2 played a completely opposite role. 39 However, Zic1 and Zic4 were highly expressed through promoter DNA demethylation in desmoid tumor, 40 which is another type of tumor with irregular activation of the Wnt signaling. 41 These studies indicate that the function of Zic family differs greatly among tumor histological types.…”

Section: Discussionmentioning

confidence: 99%

Zic1 suppresses gastric cancer metastasis by regulating Wnt/β‐catenin signaling and epithelial‐mesenchymal transition

et al. 2020

FASEB j.

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Gastric cancer (GC) patients with metastasis had limited treatment options and dismal outcome. We have previously reported the aberrant expression of Zic family member 1 (Zic1) in GC. However, the functional roles and underlying mechanism of Zic1 in GC metastasis remain unknown. Here, we demonstrate that lower expression of Zic1 was correlated with more lymph node metastasis and poor outcome of GC patients. Ectopic expression of Zic1 suppressed both lung metastasis and peritoneal tumor dissemination of GC in mice. The metastatic suppressing ability of Zic1 was mediated by regulating the process of cell invasion, adhesion and epithelial-mesenchymal transition (EMT). Mechanistically, Zic1 could downregulate Wnt targets including c-Myc and Cyclin D1 by inhibiting LEF transcriptional activity in GC cells.Notably, Zic1 was inversely related to the expression of Cyclin D1 in GC tissues tested. In addition, Zic1 could physically interact with β-catenin/transcription factor 4 (TCF4) and disrupt their complex formation, while not affecting β-catenin nuclear localization. Collectively, our study indicated that Zic1 suppressed GC metastasis through attenuating Wnt/β-catenin signaling and the EMT process. Our work may provide novel therapeutic strategies for the metastasis of GC.

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“…In recent years, more and more researches demonstrated that aerobic glycolysis plays a pivotal role in the development of colon cancer and in the treatment of colon cancer by using anticancer agent [34][35][36]. However, it is not clear whether IC261 are involved in the regulation of aerobic glycolysis in colon cancer cells.…”

Section: Discussionmentioning

confidence: 99%

IC261, a specific inhibitor of CK1δ/ε, promotes aerobic glycolysis through p53-dependent mechanisms in colon cancer

Liu¹,

Hu²,

Lu³

et al. 2020

Int. J. Biol. Sci.

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Casein kinase 1δ (CK1δ) and casein kinase 1ε (CK1ε) have been proposed to be involved in DNA replication, differentiation and apoptosis, thus participating in the regulation of tumorigenesis. However, their functions in colon cancer and the underlying mechanism remain unclear. Here, we found that the expression of CK1ε and CK1δ increased significantly in cancer tissues and the upregulation of CK1ε and CK1δ were closely related to poor differentiation, advanced TNM stage and poor prognosis of colon cancer. CK1δ/ε inhibitor IC261 could induce a decrease in cell survival and proliferation, and an increase in apoptosis in colon cancer cells. Interestingly, IC261 increased the level of aerobic glycolysis in colon cancer cells. Meanwhile, IC261 caused the decrease of p53 protein level and the misregulation of glycolysis related genes (TIGAR, G6PD, GLUT1) which are closely related to the regulation of glycolysis by p53. Inhibiting p53 by siRNA or inhibitor could significantly attenuate the upregulation of aerobic glycolysis induced by IC261. Finally, inhibition of aerobic glycolysis can further increase the cytotoxicity induced by IC261. Collectively, our results revealed that IC261 could inhibit the growth of colon cancer cells and increase the level of aerobic glycolysis, which is regulated by p53-dependent manner. This result suggested that targeting CK1δ/ε and glycolysis might be a valuable strategy treatment and combination therapies for colon cancer.

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β-Catenin/Tcf7l2–dependent transcriptional regulation of GLUT1 gene expression by Zic family proteins in colon cancer

Cited by 35 publications

References 60 publications

LncRNA TUG1 competitively binds to miR‐340 to accelerate myocardial ischemia‐reperfusion injury

LncRNA TUG1 competitively binds to miR‐340 to accelerate myocardial ischemia‐reperfusion injury

Zic1 suppresses gastric cancer metastasis by regulating Wnt/β‐catenin signaling and epithelial‐mesenchymal transition

IC261, a specific inhibitor of CK1δ/ε, promotes aerobic glycolysis through p53-dependent mechanisms in colon cancer

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