Expression and Yes-Associated Protein in Gastric Adenocarcinoma and Inhibitory Effects of its Knockdown on Gastric Cancer Cell Proliferation and Metastasis

Zhang, J; Zp, Xu; Yang, Yan-Jun; Js, Zhu; Zhou, Zun-Qiang; Wx, Chen

doi:10.1177/039463201202500304

Cited by 37 publications

(35 citation statements)

References 24 publications

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“…As a newly discovered cell signal transduction pathway, the Hippo signaling pathway has important roles in regulating the volume and size of organs (3,4). YAP upregulation has been identified in various cancer types, including ovarian, lung, liver, gastric and prostate cancer and it has been associated with tumor progression and sensitivity to chemotherapy, indicating that YAP participates in tumor development (5)(6)(7)(8)(9). YAP has been reported to contribute to the resistance of various cancer types to chemotherapy drugs (10).…”

Section: Introductionmentioning

confidence: 99%

Verteporfin enhances the sensitivity of LOVO/TAX cells to taxol via YAP inhibition

et al. 2018

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Studies have reported that taxol (TAX) is an effective drug for the treatment of colorectal cancer; however, its application inevitably results in drug resistance. Overexpression of Yes-associated protein (YAP) is considered one of the factors that cause TAX resistance, which may be inhibited by verteporfin (VP) treatment. The present study aimed to confirm the role of YAP in TAX resistance and to investigate whether the drug sensitivity of the TAX-resistant LOVO/TAX cell line to TAX is affected by VP treatment. The role of YAP in TAX resistance was first determined through vector-mediated overexpression and inhibition of YAP in cells. Reverse-transcription quantitative polymerase chain reaction and western blot analysis were performed for detection of associated mRNA and protein, respectively. An MTT assay was used to detect the drug sensitivity of cells to TAX. The results suggested that compared with that in the native LOVO cell line, YAP expression was significantly increased in LOVO/TAX cells. YAP gene silencing markedly enhanced the drug sensitivity of LOVO/TAX cells to TAX and, on the contrary, the drug sensitivity notably declined when YAP was overexpressed in LOVO cells. The results indicated that YAP gene expression and TAX resistance were correlated. VP treatment suppressed YAP expression and increased the drug sensitivity of LOVO/TAX cells to TAX in a dose-dependent manner. In addition, compared with VP alone, VP and TAX combination therapy had a greater inhibitory effect on YAP expression. VP treatment enhanced the drug sensitivity of LOVO/TAX cells to TAX through inhibiting YAP expression.

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Section: Introductionmentioning

confidence: 99%

Verteporfin enhances the sensitivity of LOVO/TAX cells to taxol via YAP inhibition

et al. 2018

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“…They are expressed on the tumour cell surface, activate pro-MMP to exacerbate the malignancy, and are considered a powerful indicator of distant metastasis of cancer [38]. Our previous study has shown that LATS1/YAP signalling involves in tumour growth and invasion through regulation of the expression of Ki-67 and MMP-2 [39]. Furthermore, our present finding showed that, 17-AAG inhibited LAC cell growth and invasion with the decreased expression of Ki-67 and MMP-2, suggesting that LATS1/YAP signalling might mediate 17-AAG suppression of tumour growth and invasion via regulation of Ki-67 and MMP-2 expression in LAC cells.…”

Section: Discussionmentioning

confidence: 99%

17‐AAG suppresses growth and invasion of lung adenocarcinoma cells via regulation of the LATS1/YAP pathway

Luo

et al. 2015

J Cellular Molecular Medi

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The large tumour suppressor 1 (LATS1) signalling network has been proved to be an essential regulator within the cell, participating in multiple cellular phenotypes. However, it is unclear concerning the clinical significance of LATS1 and the regulatory mechanisms of 17-Allylamino-17- demethoxygeldanamycin (17-AAG) in lung adenocarcinoma (LAC). The aim of the present study was to investigate the correlation of LATS1 and yes-associated protein (YAP) expression with clinicopathological characteristics in LAC patients, and the effects of 17-AAG on biological behaviours of LAC cells. Subcutaneous LAC tumour models were further established to observe the tumour growth in nude mice. The results showed that the positive expression of LATS1 was significantly lowered (26.7% versus 68.0%, P < 0.001), while that of YAP was elevated (76.0% versus 56.0%, P + 0.03) in LAC tissues compared to the adjacent non-cancerous tissues; LAST1 expression was negatively correlated with YAP expression (r + 0.432, P < 0.001) and lymphatic invasion of the tumour (P + 0.015). In addition, 17-AAG inhibited proliferation and invasion, and induced cell apoptosis and cycle arrest in LAC cells together with increased expression of E-cadherin and p-LATS1, and decreased expression of YAP and connective tissue growth factor. Tumour volumes and weight were much smaller in 17-AAG-treated groups than those in untreated group (P < 0.01). Taken together, our findings indicate that decreased expression of LATS1 is associated with lymphatic invasion of LAC, and 17-AAG suppresses growth and invasion of LAC cells via regulation of the LATS1/YAP pathway in vitro and in vivo, suggesting that we may provide a promising therapeutic strategy for the treatment of human LAC.

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“…However, a growing body of evidence indicates that YAP and TAZ also play a role in gastric cancer. YAP expression is commonly observed in GC samples and GC cell lines, and its expression and nuclear localization correlate with poor prognosis (Kang et al, 2011;Song et al, 2012;Zhang et al, 2012). Relevantly, YAP expression in the GC cell line MKN-28 modulates actin remodeling and promotes cell migration, while the loss of YAP induces cell stiffening and impaired migration (Qiao et al, 2017).…”

Section: Future Directions and Conclusionmentioning

confidence: 99%

Wnt5a Signaling in Gastric Cancer

Astudillo

2020

Front. Cell Dev. Biol.

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Gastric cancer remains an important health challenge, accounting for a significant number of cancer-related deaths worldwide. Therefore, a deeper understanding of the molecular mechanisms involved in gastric cancer establishment and progression is highly desirable. The Wnt pathway plays a fundamental role in development, homeostasis, and disease, and abnormal Wnt signaling is commonly observed in several cancer types. Wnt5a, a ligand that activates the non-canonical branch of the Wnt pathway, can play a role as a tumor suppressor or by promoting cancer cell invasion and migration, although the molecular mechanisms explaining these roles have not been fully elucidated. Wnt5a is increased in gastric cancer samples; however, most gastric cancer cell lines seem to exhibit little expression of this ligand, thus raising the question about the source of this ligand in vivo. This review summarizes available research about Wnt5a expression and signaling in gastric cancer. In gastric cancer, Wnt5a promotes invasion and migration by modulating integrin adhesion turnover. Disheveled, a scaffolding protein with crucial roles in Wnt signaling, mediates the adhesion-related effects of Wnt5a in gastric cancer cells, and several studies provide growing support for a model whereby Disheveled-interacting proteins mediates Wnt5a signaling to modulate cytoskeleton dynamics. However, Wnt5a might induce other effects in gastric cancer cells, such as cell survival and induction of gene expression. On the other hand, the available evidence suggests that Wnt5a might be expressed by cells residing in the tumor microenvironment, where feedback mechanisms sustaining Wnt5a secretion and signaling might be established. This review analyzes the possible functions of Wnt5a in this pathological context and discusses potential links to mechanosensing and YAP/TAZ signaling.

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Expression and Yes-Associated Protein in Gastric Adenocarcinoma and Inhibitory Effects of its Knockdown on Gastric Cancer Cell Proliferation and Metastasis

Cited by 37 publications

References 24 publications

Verteporfin enhances the sensitivity of LOVO/TAX cells to taxol via YAP inhibition

Verteporfin enhances the sensitivity of LOVO/TAX cells to taxol via YAP inhibition

17‐AAG suppresses growth and invasion of lung adenocarcinoma cells via regulation of the LATS1/YAP pathway

Wnt5a Signaling in Gastric Cancer

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