Ophiopogonin B induces reactive oxygen species‑dependent apoptosis through the Hippo pathway in nasopharyngeal carcinoma

Dong, Wenhui; Dong, Qing; Ding, Hairui

doi:10.3892/mmr.2021.12173

Cited by 13 publications

(8 citation statements)

References 41 publications

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“…After determining the function of lncRNA-LUADT1 in NPC, we further explored the molecular mechanism of its involvement. It has been shown that the Hippo/YAP signaling pathway is involved in the development of NPC [ 20 ]. Subsequently, Western blot detection verifies the expression level of LATS1 in the si-LUADT1 group was distinctly higher, while the expression of YAP1, TAZ, and TEAD1 were significantly lower compared with the si-NC group ( Figure 2(f )), displaying that knocking down lncRNA-LUADT1 can inhibit Hippo/YAP signaling pathway activation.…”

Section: Resultsmentioning

confidence: 99%

“…Current research has indicated that this signaling pathway is activated in human liver cancer tissues [ 35 ], lung cancer tissues [ 36 ], colorectal cancer tissues [ 37 ], ovarian cancer tissues [ 38 ], and other tumor tissues. At present, studies have shown that Ophiopogon saponins B pass through the Hippo pathway to induce cell apoptosis in NPC dependent on reactive oxygen, suggesting an involvement of the Hippo pathway NPC development [ 20 ]. In the research conducted this study, it was acquired that by interfering with lncRNA-LUADT1 expression, NPC cells saw an up-regulation in the LATS1 protein.…”

Section: Discussionmentioning

confidence: 99%

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Long non-coding RNA LUADT1 promotes nasopharyngeal carcinoma cell proliferation and invasion by downregulating miR-1207-5p

Jiang

Zhao

et al. 2021

Bioengineered

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Nasopharyngeal carcinoma (NPC) is a typical type of malignant tumor. This research paper aims to study the function and mechanism of long non-coding RNA lung adenocarcinoma-related transcript 1 (lncRNA-LUADT1) in the progression of NPC. In this study, the expressions of lncRNA-LUADT1, miR-1207-5p, and TEAD1 in NPC tissues and cell lines were detected by RT-qPCR. Initially, the expression of lncRNA-LUADT1 and TEAD1 were significantly up-regulated in NPC tissues and cells, while miR-1207-5p was significantly down-regulated. Next, miR-1207-5p was confirmed to bind to lncRNA-LUADT1 or TEAD1 by bioinformatics and luciferase reporter assay. In addition, after interfering with lncRNA-LUADT1 expression, experiments of CCK8, EDU staining, and Transwell invasion were used to detect proliferation, invasion, and migration of NPC cells. The results showed that interfering with lncRNA-LUADT1 expression could inhibit the proliferation, invasion, and migration of NPC cells. Western blot showed that lncRNA-LUADT1 knockdown significantly decreased the expression of Hippo/YAP pathway protein (YAP1 and TAZ). However, interfering with the expression of miR-1207-5p reversed these results. In addition, the nude mouse tumor formation experiment suggested that low-expressed lncRNA-LUADT1 reduced the volume and weight of tumor tissues. In summary, lncRNA-LUADT1 down-regulation could inhibit NPC cell proliferation and invasion, which may be achieved through regulating miR-1207-5p expression and affecting TEAD1 expression, thus inhibiting the activation of Hippo/YAP signaling pathway.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA LUADT1 promotes nasopharyngeal carcinoma cell proliferation and invasion by downregulating miR-1207-5p

Jiang

Zhao

et al. 2021

Bioengineered

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“…Investigation of changes in intracellular activity of incubated cells with compound 142 using the Western blot method resulted in increased protein expression levels of caspase 3 and B-cell lymphoma 2 (Bcl-2)-associated X protein [ 208 ]. Compound 142 also inhibited the proliferation of NPC cells by inducing apoptosis and disturbing the mitochondrial integrity [ 209 ]. In addition, compound 142 promotes the expression of mammalian STE20-like kinase 1, large tumor suppressor 1, and phosphorylated-associated protein (YAP), suppresses the expression of YAP and transcriptionally enhances associate domains in NPC cells ( Figure 31 ) [ 209 ].…”

Section: Heterocyclic Compoundsmentioning

confidence: 99%

“…Compound 142 also inhibited the proliferation of NPC cells by inducing apoptosis and disturbing the mitochondrial integrity [ 209 ]. In addition, compound 142 promotes the expression of mammalian STE20-like kinase 1, large tumor suppressor 1, and phosphorylated-associated protein (YAP), suppresses the expression of YAP and transcriptionally enhances associate domains in NPC cells ( Figure 31 ) [ 209 ].…”

Section: Heterocyclic Compoundsmentioning

confidence: 99%

Synthetic and Naturally Occurring Heterocyclic Anticancer Compounds with Multiple Biological Targets

et al. 2021

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Cancer is a complex group of diseases initiated by abnormal cell division with the potential of spreading to other parts of the body. The advancement in the discoveries of omics and bio- and cheminformatics has led to the identification of drugs inhibiting putative targets including vascular endothelial growth factor (VEGF) family receptors, fibroblast growth factors (FGF), platelet derived growth factors (PDGF), epidermal growth factor (EGF), thymidine phosphorylase (TP), and neuropeptide Y4 (NY4), amongst others. Drug resistance, systemic toxicity, and drug ineffectiveness for various cancer chemo-treatments are widespread. Due to this, efficient therapeutic agents targeting two or more of the putative targets in different cancer cells are proposed as cutting edge treatments. Heterocyclic compounds, both synthetic and natural products, have, however, contributed immensely to chemotherapeutics for treatments of various diseases, but little is known about such compounds and their multimodal anticancer properties. A compendium of heterocyclic synthetic and natural product multitarget anticancer compounds, their IC50, and biological targets of inhibition are therefore presented in this review.

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“…Given most TEAD proteins are involved in gastrointestinal carcinoma such as esophageal and gastric cancers, 5 the TEAD4 was also reported to closely associate with the tumorigenesis of nasopharyngeal cancer (NPC) 6,7 . For example, the binding of YAP1 to TEAD4 was revealed to promote tumor invasion and metastasis in NPC with hepatitis virus infection, 8 which was also found to be responsible for cisplatin resistant‐induced epithelial‐mesenchymal transition 9 and ophiopogonin‐induced reactive oxygen species‐dependent apoptosis in NPC cells 10 . In recent years, the YAP1‐TEAD4 interaction has been recognized as an attractive druggable target, and molecular disruption of the interaction can inactivate the TEAD4 signaling as a potential therapeutic strategy against NPC and some other cancers 11 .…”

Section: Introductionmentioning

confidence: 99%

Molecular design and rational optimization of synergistic effect between the two wings of a roughly orthogonal cation‐π‐π stacking system at nasopharyngeal carcinoma YAP1‐TEAD4 parallel Helix‐Helix interaction interface

Zhu

et al. 2022

J of Molecular Recognition

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The Yes-associated protein-1 (YAP1) is an essential regulator of human Hippo signaling pathway and functions through interaction with TEA domain-4 (TEAD4) transcription factor involved in the tumorigenesis of nasopharyngeal cancer. Previously, a parallel helix-helix interaction (PHHI) was identified as the key hotspot at YAP1-TEAD4 complex interface and has been exploited as an attractive druggable target to disrupt the complex. In this study, we investigated a roughly orthogonal cation-π-π stacking system across the crystal PHHI packing interface by integrating computational modeling and binding assay, which forms between one YAP1 helical residue Phe69 and two TEAD4 helical residues Phe373/Lys376. A synergistic effect between cation-π and π-π interactions was observed; they separately represent two wings of the stacking system. The π-electron is primarily responsible for the synergistic effect. Combination between diverse aromatic/charged amino acids. as well as neutral alanine on the cation-π-π stacking, revealed that the presence of aromatic tryptophan and charged arginine at, respectively, the residues 373 and 376 of TEAD4 helix can considerably improve PHHI binding affinity by $6-fold, whereas neutral alanine substitution on each residue and on both would reduce the affinity significantly, confirming a strong synergistic effect involved in the roughly orthogonal cation-π-π stacking system at YAP1-TEAD4 PHHI interface.

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Ophiopogonin B induces reactive oxygen species‑dependent apoptosis through the Hippo pathway in nasopharyngeal carcinoma

Cited by 13 publications

References 41 publications

Long non-coding RNA LUADT1 promotes nasopharyngeal carcinoma cell proliferation and invasion by downregulating miR-1207-5p

Long non-coding RNA LUADT1 promotes nasopharyngeal carcinoma cell proliferation and invasion by downregulating miR-1207-5p

Synthetic and Naturally Occurring Heterocyclic Anticancer Compounds with Multiple Biological Targets

Molecular design and rational optimization of synergistic effect between the two wings of a roughly orthogonal cation‐π‐π stacking system at nasopharyngeal carcinoma YAP1‐TEAD4 parallel Helix‐Helix interaction interface

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