Suppression of SIPA-1 expression may reduce bladder cancer invasion and metastasis via the downregulation of E-cadherin and ZO-1

Zhang, Ping; Wang, Xinghuan

doi:10.3892/etm.2015.2891

Cited by 4 publications

(3 citation statements)

References 34 publications

(43 reference statements)

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“…Down-regulation of E-cadherin leads to the decrease of intercellular adhesion junctions, the decrease of polarity and the transformation of cells from epithelioid to interstitial, which is one of the important markers of epithelial–mesenchymal transition (EMT) [26]. At the same time, EMT can promote the migration of tumor cells, enhance the invasion of tumor cells, and promote the occurrence of metastases [27,28]. E-cadherin has a certain correlation with the occurrence of many kinds of tumors.…”

Section: Discussionmentioning

confidence: 99%

Ribophorin II promotes cell proliferation, migration, and invasion in esophageal cancer cells in vitro and in vivo

Huang

Bai

et al. 2019

Bioscience Reports

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Esophageal cancer is a common digestive tract cancer, which is a serious threat to human health. Ribophorin II (RPN2) is a part of an N-oligosaccharyltransferase complex, which is excessively expressed in many kinds of cancers. In the present study, we explore the biological role of RNP2 in esophageal cancer. First, we found that the expression of RPN2 was higher in esophageal cancer tissues than in adjacent non-tumor tissues, and negatively correlated with E-cadherin expression. RPN2 expression levels in esophageal cancer tissues were positively associated with differentiation and tumor node metastasis (TNM) stage. Furthermore, the expression of RPN2 was increased significantly in esophageal cancer cell lines compared with normal cells. The effect of RPN2 down-regulation on cell proliferation, cell migration, and cell invasion was examined by cell counting kit-8 (CCK8), wound healing assay, and Transwell assay, respectively. Silencing RPN2 effectively inhibited cell proliferation of esophageal cancer cells in vitro and in vivo. Cell migration and invasion were also weakened dramatically by siRPN2 treatment of esophageal cancer cells. In addition, protein expression of proliferating cell nuclear antigen (PCNA), matrix metalloproteinase (MMP-2), and E-cadherin in esophageal cancer cells was determined by Western blot analysis. PCNA, MMP-2, E-cadherin, Snail and phosphorylation-Smad2/3 expression was also regulated notably by siRPN2 treatment. These findings indicate that RPN2 exhibits oncogenetic capabilities in esophageal cancer, which could provide novel insights into esophageal cancer prevention and treatment.

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Section: Discussionmentioning

confidence: 99%

Ribophorin II promotes cell proliferation, migration, and invasion in esophageal cancer cells in vitro and in vivo

Huang

Bai

et al. 2019

Bioscience Reports

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“…Decreased expression of E-cadherin in bladder cancer tissues mediates cell migration and invasion. 21 MMP-2 and MMP-9 are important factors responsible for cancer cell migration and invasion. 22 , 23 In our study, the expression of E-cadherin, MMP-2, and MMP-9 was detected by Western blotting.…”

Section: Discussionmentioning

confidence: 99%

Nodal regulates bladder cancer cell migration and invasion via the ALK/Smad signaling pathway

Zhong

Zhu

et al. 2018

OTT

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BackgroundBladder cancer is the most common malignant tumor of the urinary tract. We aimed to explore the biological role and molecular mechanism of Nodal in bladder cancer.Materials and methodsThe expression of Nodal in bladder cancer tissues and cells was determined by quantitative real-time polymerase chain reaction. The effect of silencing of Nodal on cell proliferation, clone formation, and migration and invasion was evaluated by MTT cell proliferation assay, colony formation, and transwell assays, respectively. Western blot analysis was employed to detect the expression of proliferation- and invasion-related proteins and proteins involved in ALK/Smad signaling.ResultsWe found that the expression of Nodal was significantly increased in bladder cancer tissues and cell lines. Downregulation of Nodal effectively weakened cell proliferation, clone formation, and cell migration and invasion abilities. The protein expression levels of CDC6, E-cadherin, MMP-2, and MMP-9 were also altered by downregulation of Nodal. Knockdown of Nodal also blocked the expression of ALK4, ALK7, Smad2, and Smad4, which are involved in ALK/Smad signaling. Additionally, the ALK4/7 receptor blocker SB431542 reversed the promotive effects of Nodal overexpression on bladder cancer cell proliferation, migration, and invasion.ConclusionOur study indicated that Nodal functions as an oncogene by regulating cell proliferation, migration, and invasion in bladder cancer via the ALK/Smad signaling pathway, thereby providing novel insights into its role in bladder cancer treatment.

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“…Babkair H et al indicated that aberrant expression of claudin‐1 and ZO‐1 mediated cell growth and invasion in oral squamous cell carcinoma . Zhang P et al found that the suppression of SIPA‐1 expression might reduce bladder cancer invasion and metastasis via the upregulation of E‐cadherin and ZO‐1 . All these studies showed that inhibition of the expression of cell junction‐associated proteins was sufficient to cause tumor invasion and metastasis.…”

Section: Discussionmentioning

confidence: 99%

Tumor‐derived exosomes enhance invasion and metastasis of salivary adenoid cystic carcinoma cells

Hou

Wang

Liu

et al. 2017

J Oral Pathology Medicine

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Suppression of SIPA-1 expression may reduce bladder cancer invasion and metastasis via the downregulation of E-cadherin and ZO-1

Cited by 4 publications

References 34 publications

Ribophorin II promotes cell proliferation, migration, and invasion in esophageal cancer cells in vitro and in vivo

Ribophorin II promotes cell proliferation, migration, and invasion in esophageal cancer cells in vitro and in vivo

Nodal regulates bladder cancer cell migration and invasion via the ALK/Smad signaling pathway

Tumor‐derived exosomes enhance invasion and metastasis of salivary adenoid cystic carcinoma cells

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