Knockdown of YAP inhibits growth in Hep-2 laryngeal cancer cells via epithelial-mesenchymal transition and the Wnt/β-catenin pathway

Tang, Xiaomin; Sun, Yuxuan; Wan, Ganglun; Sun, Jiaqiang; Sun, Jingwu; Pan, Chensheng

doi:10.1186/s12885-019-5832-9

Cited by 30 publications

(16 citation statements)

References 30 publications

(32 reference statements)

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“…Furthermore, YAP was reported to contribute to tumor initiation, progression and metastasis ( 37 ). Tang et al ( 38 ) demonstrated that the expression of β-catenin was markedly reduced after YAP downregulation in laryngeal cancer cells. Wang et al ( 39 ) also reported that P-YAP contributed to the degradation of β-catenin in colorectal cancer cells.…”

Section: Discussionmentioning

confidence: 99%

CBX2 depletion inhibits the proliferation, invasion and migration of gastric cancer cells by inactivating the YAP/β-catenin pathway

Zeng

Yang

et al. 2020

Mol Med Rep

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Gastric cancer (GC) is the most common and fast-growing malignancy of the digestive system, which has a high mortality. Chromobox homolog 2 (CBX2) has been reported to be highly expressed in cancer tissues compared with adjacent normal tissues. It has also been established that CBX2 is upregulated in GC cell lines by searching the Cancer Cell Line Encyclopedia. The aim of the present study was to investigate the biomolecular role and underlying mechanism of CBX2 in the proliferation, invasion and migration of GC cells. Short hairpin RNA-CBX2 and yes-associated protein (YAP) overexpression plasmids were constructed to regulate CBX2 and YAP expression, respectively. Additionally, the expression of certain mRNAs and proteins involved in the YAP/β-catenin pathway and those associated with cell invasion were assessed by western blotting and reverse transcription-quantitative PCR, respectively. The cellular behaviors of MFC cells were analyzed using Cell Counting Kit-8, colony formation wound-healing and Transwell assays. The results of the present study revealed that increased CBX2 expression was observed in GC cell lines compared with normal gastric cells. In addition, CBX2 knockdown inhibited the nuclear cytoplasm translocation of YAP, inducing its phosphorylation, and suppressing the activation of the β-catenin signaling pathway. The results also demonstrated that CBX2 depletion inhibited the proliferation, migration and invasion of GC cells by inactivating the YAP/β-catenin pathway. It was determined that CBX2 promoted the proliferation, invasion and migration of GC cells by activating the YAP/β-catenin pathway, suggesting that CBX2 is involved in the pathogenesis of GC and may represent a novel target for the clinical treatment of GC.

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Section: Discussionmentioning

confidence: 99%

CBX2 depletion inhibits the proliferation, invasion and migration of gastric cancer cells by inactivating the YAP/β-catenin pathway

Zeng

Yang

et al. 2020

Mol Med Rep

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“…Wnt/ β-catenin downregulation is helpful to reduce LCA cell malignant episodes. 39 Taken together, miR-139-3p overexpression curtails LCA cell growth and promotes cancer cell apoptosis via the KDM5B-mediated SOX2/Wnt/βcatenin axis.…”

Section: Dovepressmentioning

confidence: 97%

<p>microRNA-139-3p Inhibits Malignant Behaviors of Laryngeal Cancer Cells via the KDM5B/SOX2 Axis and the Wnt/β-Catenin Pathway</p>

Ma¹,

Chen²,

Yu³

2020

CMAR

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Background: Laryngeal cancer (LCA) is a common head and neck cancer. Lysine demethylase 5B (KDM5B) knockdown is expected as a new target for cancer prevention. We investigated the molecular mechanism of KDM5B in LCA. Materials and Methods: The levels of KDM5B, microRNA (miR)-139-3p and highmobility-group box 2 (SOX2) in LCA tissues and cells, normal tissues and cells were detected. The effect of KDM5B on LCA was evaluated. The upstream miR of KDM5B and the downstream gene and pathway of KDM5B were predicted and their effects on LCA were analyzed. The Wnt/β-catenin pathway-specific activator agonist was delivered into LCA cells expressing miR-139-3p mimic to evaluate the role of the Wnt/β-catenin pathway. Results: KDM5B was highly expressed in LCA, and inhibition of KDM5B suppressed LCA progression. miR-139-3p, downregulated in LCA tissues, was a regulatory miR of KDM5B. Overexpression of miR-139-3p significantly inhibited the malignant biological behaviors of LCA cells. KDM5B promoted SOX2 expression via histone demethylation. SOX2 was highly expressed in LCA, and overexpression of SOX2 promoted LCA progression by inducing the Wnt/β-catenin pathway. Activated Wnt/β-catenin pathway attenuated the inhibitory effect of miR-139-3p mimic on the malignant biological behaviors of LCA cells. Conclusion: miR-139-3p overexpression inhibited LCA development via regulating the KDM5B/SOX2 axis and inhibiting the Wnt/β-catenin pathway.

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“…In 3T3-L1 cells, disruption of the YAP/TAZ and TEAD interaction by VP treatment significantly reduced DKK1 mRNA, and knockdown of TEAD reduced DKK1 levels 39 . In Hep-2 cells, the expression of DKK1 was significantly decreased after YAP downregulation 40 . There may indeed be a feedback loop.…”

Section: Discussionmentioning

confidence: 96%

Dickkopf-1 promotes Vascular Smooth Muscle Cell proliferation and migration through upregulating UHRF1 during Cyclic Stretch application

Zheng¹,

Liu²,

Li³

et al. 2021

Int. J. Biol. Sci.

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Dickkopf-1 (DKK1) was recently shown to play an important role in cardiovascular disease. The aim of this work was to assess the role of DKK1 in the regulation of smooth muscle cell function by mechanical stretch and the mechanisms underlying this process. Methods: Wild-type C57BL/6J mice were subjected to sham or abdominal aortic constriction (AAC) surgery. The expression level of DKK1 was examined by immunohistochemical staining and Western blotting. Analyses of DKK1 function in vascular smooth muscle cell (VSMC) proliferation and migration were performed. Transcriptome sequencing analysis was performed to identify the differentially expressed genes and pathways regulated by DKK1. Smooth muscle-specific Dkk1 knockout mice were used to confirm the function of DKK1 in vivo . Chromatin immunoprecipitation (ChIP) was used to confirm DNA-protein interactions. Promoter luciferase analysis was used to detect transcription factor activity. Results: We found that AAC significantly increased DKK1 protein levels in the thoracic aorta and coronary artery in vivo . In vitro , high-level stretch (18%) induced the expression of DKK1 in VSMCs. Knocking down DKK1 inhibited VSMC proliferation and migration under high-level stretch (18%). We identified ubiquitin-like containing PHD and RING finger domains 1 (UHRF1) as a target gene of DKK1. Knockdown of UHRF1 with small interfering RNAs partially reversed the regulatory effect of recombinant DKK1 on VSMCs. Specific deletion of DKK1 in VSMCs was sufficient to attenuate the AAC-induced upregulation of UHRF1, thickening of arterial media and increase in VSMC proliferation. Furthermore, we found that DKK1 regulated UHRF1 expression through the YAP-TEAD pathway. TEAD1 and TEAD4 bound directly to the promoter of UHRF1, and blocking the YAP-TEAD interaction inhibited UHRF1 upregulation due to DKK1. Conclusions: This study reveals that DKK1 mediates the mechanical stretch regulation of smooth muscle cell function by modulating UHRF1 expression through the YAP-TEAD pathway.

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Knockdown of YAP inhibits growth in Hep-2 laryngeal cancer cells via epithelial-mesenchymal transition and the Wnt/β-catenin pathway

Cited by 30 publications

References 30 publications

CBX2 depletion inhibits the proliferation, invasion and migration of gastric cancer cells by inactivating the YAP/β-catenin pathway

CBX2 depletion inhibits the proliferation, invasion and migration of gastric cancer cells by inactivating the YAP/β-catenin pathway

<p>microRNA-139-3p Inhibits Malignant Behaviors of Laryngeal Cancer Cells via the KDM5B/SOX2 Axis and the Wnt/β-Catenin Pathway</p>

Dickkopf-1 promotes Vascular Smooth Muscle Cell proliferation and migration through upregulating UHRF1 during Cyclic Stretch application

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