P21-activated kinase 7 (PAK7) interacts with and activates Wnt/β-catenin signaling pathway in breast cancer

Li, Kai; Xu, Xiaolong; He, Yanqi; Tian, Yihao; Pan, Wenting; Liu, Xu; Ma, Yayun; Gao, Yang; Gao, Jinliang; Qi, Yuwen; Wei, Lei; Zhang, Jingwei

doi:10.7150/jca.24934

Cited by 26 publications

(17 citation statements)

References 55 publications

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“…We also quantified the percentage of wound healing via image processing (Figure B). Previous studies consistently reported that, in the same cell populations, mesenchymal phenotypes have a higher rate of migration and fill the scratch in a shorter time when compared to epithelial phenotypes. , …”

Section: Resultsmentioning

confidence: 82%

Nanostructured Architectures Promote the Mesenchymal–Epithelial Transition for Invasive Cells

et al. 2020

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Dynamic modulation of cellular phenotypes between the epithelial and mesenchymal statesthe epithelial–mesenchymal transition (EMT) and mesenchymal–epithelial transition (MET)plays an important role in cancer progression. Nanoscale topography of culture substrates is known to affect the migration and EMT of cancer cells. However, existing platforms heavily rely on simple geometries such as grooved lines or cylindrical post arrays, which may oversimplify the complex interaction between cells and nanotopography in vivo. Here, we use electrodeposition to construct finely controlled surfaces with biomimetic fractal nanostructures as a means of examining the roles of nanotopography during the EMT/MET process. We found that nanostructures in the size range of 100 to 500 nm significantly promote MET for invasive breast and prostate cancer cells. The “METed” cells acquired distinct expression of epithelial and mesenchymal markers, displayed perturbed morphologies, and exhibited diminished migration and invasion, even after the removal of a nanotopographical stimulus. The phosphorylation of GSK-3 was decreased, which further tuned the expression of Snail and modulated the EMT/MET process. Our findings suggest that invasive cancer cells respond to the geometries and dimensions of complex nanostructured architectures.

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Section: Resultsmentioning

confidence: 82%

Nanostructured Architectures Promote the Mesenchymal–Epithelial Transition for Invasive Cells

et al. 2020

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“…The results of the CCK‐8 assay showed that overexpression of GMDS‐AS1 significantly inhibited the proliferation of cells (Figure G,H), which were consistent with the results of colony formation assay (Figure I,J). Cyclin A1 and cyclin B1 belong to the cyclin family, which accelerate the cell cycle by interacting with cyclin‐dependent kinases (CDKs) . Therefore, upregulation of cyclin A1 and cyclin B1 expression levels can promote cell proliferation.…”

Section: Resultsmentioning

confidence: 99%

LncRNA GMDS‐AS1 inhibits lung adenocarcinoma development by regulating miR‐96‐5p/CYLD signaling

Zhao

Zhang

et al. 2019

Cancer Medicine

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According to the global cancer statistic, lung cancer is one of the most dangerous tumors, which poses a serious threat to human health. Exploration the mechanism of lung cancer and new targeted therapeutic measures is always the hot topic. Long noncoding RNA (lncRNA) is an important factor affecting the development of tumors. However, the research on the mechanism of lncRNA in the progress of lung cancer needs to be further expanded. In this study, we found that the expression of lncRNA GMDS‐AS1 was significantly reduced in lung adenocarcinoma (LUAD) tissues and cells. Upregulated GMDS‐AS1 can significantly inhibit the proliferation of LUAD cells and promote cell apoptosis in vitro and in vivo. The results indicate that GMDS‐AS1 acts as a tumor suppressor gene to affect the development of LUAD. Further studies revealed that GMDS‐AS1 is a target gene of miR‐96‐5p, and GMDS‐AS1 regulates proliferation and apoptosis of LUAD cells in association with miR‐96‐5p. In addition, we also confirmed that CYLD lysine 63 deubiquitinase (CYLD) is also a target gene of miR‐96‐5p. Through various validations, we confirmed that GMDS‐AS1 can act as a ceRNA to upregulate the expression of CYLD by sponging miR‐96‐5p. Moreover, the intervention of GMDS‐AS1/miR‐96‐5p/CYLD network can regulate the proliferation and apoptosis of LUAD cells. In this study, we revealed that the GMDS‐AS1/miR‐96‐5p/CYLD network based on ceRNA mechanism plays an important role in the development of LUAD and provides a new direction and theoretical basis for targeted therapy of LUAD.

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“…The TOP/FOP flash assay is a reporter gene assay used to detect Wnt/β‐catenin signaling pathway activity . The TOP flash reporter plasmid contains a wild‐type (CCTTTGATC) TCF/LEF binding site, and the FOP flash reporter plasmid contains a muted (CCTTTGGCC) TCF/LEF binding site.…”

Section: Methodsmentioning

confidence: 99%

A novel tumor suppressor SPINK5 targets Wnt/β‐catenin signaling pathway in esophageal cancer

Wang

Bian

et al. 2019

Cancer Medicine

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Esophageal cancer is one of the most common tumor in the world, and the morbidity rate is as high as 100/100 000 in some parts of China. Therefore, it is important and urgent to explore the pathogenesis of esophageal cancer and find new therapeutic targets for esophageal cancer. In this study, we found that a novel tumor suppressor SPINK5 is significantly reduced in the development of esophageal cancer, and is closely related to the pathological differentiation and lymph node metastasis of esophageal cancer via bioinformatics analysis and esophageal cancer tissue array. Further studies have found that SPINK5 is closely related to Wnt/β‐catenin signaling pathway by bioinformatics analysis and western blot. In esophageal cancer cells, SPINK5 overexpression can inhibit Wnt/β‐catenin signaling pathway. Combined with LiCl or MG‐132 treatment, SPINK5 can inhibit GSK3β phosphorylation and promote β‐catenin protein degradation, thus inhibit Wnt/β‐catenin signaling pathway. In vivo study, SPINK5 overexpression can significantly inhibit the growth of esophageal cancer cells. Our study shows that SPINK5 can inhibit the proliferation, migration, and invasion of esophageal cancer cells by inhibiting Wnt/β‐catenin signaling pathway, and thus plays an important role in the development of esophageal cancer, and may serve as a treatment target of esophageal cancer.

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P21-activated kinase 7 (PAK7) interacts with and activates Wnt/β-catenin signaling pathway in breast cancer

Cited by 26 publications

References 55 publications

Nanostructured Architectures Promote the Mesenchymal–Epithelial Transition for Invasive Cells

Nanostructured Architectures Promote the Mesenchymal–Epithelial Transition for Invasive Cells

LncRNA GMDS‐AS1 inhibits lung adenocarcinoma development by regulating miR‐96‐5p/CYLD signaling

A novel tumor suppressor SPINK5 targets Wnt/β‐catenin signaling pathway in esophageal cancer

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