Tight Junctions in Human Urinary Bladder Cancer

Martin, Tracey Amanda; Haynes, Mark D.; Answare, Ninaard; Brown, Gareth; Jiang, Wen Guo

doi:10.1007/978-94-007-6028-8_6

Cited by 3 publications

(3 citation statements)

References 62 publications

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“…13,14 Abnormal claudin protein expression changes the normal structure and function of tight junctions to cause the loss of cell polarity and the diffusion of nutrients and other factors necessary for the survival and growth of tumor cells; these effects play an important role in the metastasis and nutrition supply of tumor cells. 15 Claudin protein expression is different in several types of cancer tissues, and some claudin proteins are downregulated or not expressed in cancer tissues.…”

Section: Discussionmentioning

confidence: 99%

Expression and Clinical Significance of Claudin-7 in Patients With Colorectal Cancer

Wang

et al. 2018

Technol Cancer Res Treat

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Background and Objective:Claudin-7 is a component of tight junctions and plays important roles in maintaining cell polarity and tightly connecting the barriers between cells. Abnormal claudin-7 protein expression is closely related to tumor occurrence, development, and metastasis. This study aimed to investigate the correlation between claudin-7 expression and carcinogenesis or metastasis in colorectal cancer and the clinical significance of these relationships.Materials and Methods:In this study, enzyme linked immunosorbent assays (ELISA) were used to measure the claudin-7 levels in serum from patients with colorectal cancer. Immunohistochemical staining and Western blotting were used to measure claudin-7 expression in colorectal cancer tissues, paracancerous tissues, and metastatic tissues.Results:Serum claudin-7 levels were significantly lower in patients with colorectal cancer than in healthy controls. Immunohistochemistry indicated that claudin-7 expression was lower in colorectal cancer tissues than in normal colorectal tissues, and its expression level was positively correlated with the degree of colorectal cancer tissue differentiation. Claudin-7 expression levels were significantly reduced or undetectable in metastatic tissues compared to primary tumor tissues, but there were no significant differences in claudin-7 expression among different metastatic tissues.Conclusion:We confirmed that claudin-7 downregulation was associated with colorectal cancer and metastasis. Claudin-7 could be a tumor suppressor gene for colorectal cancer and may thus serve an early diagnostic marker and a novel therapeutic target.

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Section: Discussionmentioning

confidence: 99%

Expression and Clinical Significance of Claudin-7 in Patients With Colorectal Cancer

Wang

et al. 2018

Technol Cancer Res Treat

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“…Some of these genes, such as VEGF, SRC , and MMP , have been identified as either promoting genes or suppressing genes. 1,2 However, our knowledge of the molecular mechanism underlying metastasis is far from sufficient. We still lack efficient therapies to control metastasis effectively.…”

Section: Introductionmentioning

confidence: 99%

High-Content Functional Screening of AEG-1 and AKR1C2 for the Promotion of Metastasis in Liver Cancer

Liu

Zhang

et al. 2016

SLAS Discovery

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Liver cancer is one of the most lethal cancer types in humans, but our understanding of the molecular mechanisms underlying this process remains insufficient. Here, we conducted high-content screening of the potential genes involved in liver cancer metastasis, which we selected from the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway database, based on the SAMcell method and RNA interference technology. We identified two powerful genes in the liver cancer metastasis process, AEG-1 and AKR1C2, both of which proved to be positive regulators in promoting metastasis in liver cancer. Further clinical results verified their roles in liver cancer. In summary, these findings could provide new insight into the liver cancer mechanism and potentially therapeutic novel targets for liver cancer therapies in the future.

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“…Those processes are interactive with several pathways such as cell proliferation and angiogenesis. It is suggestive that there is a systematic gene network underlying this process ( 5 ). A few factors have been identified, such as KISS1, VEGF, and MMP, as positive or negative regulators ( 6–8 ).…”

Section: Introductionmentioning

confidence: 99%

AEG-1 Promotes Metastasis Through Downstream AKR1C2 and NF1 in Liver Cancer

Wu²,

Zhang³

et al. 2015

oncol res

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Liver cancer is one of the most lethal cancers, but our knowledge of the molecular mechanism underlying this process remains insufficient. Through deep sequencing and expression regulation analysis in liver cancer cells, we identified two novel factors, AKR1C2 (positive factor) and NF1 (negative factor), as the AEG-1 downstream players in the process of metastasis in liver cancer. They were experimentally validated to have the capacities of regulating cell migration, cell invasion, cell proliferation, and EMT. Further clinic expression and animal model evidence confirmed their functions. Together, our findings provide a new insight into the pharmaceutical and therapeutic use of AEG-1 and downstream AKR1C2 and NF1.

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Tight Junctions in Human Urinary Bladder Cancer

Cited by 3 publications

References 62 publications

Expression and Clinical Significance of Claudin-7 in Patients With Colorectal Cancer

Expression and Clinical Significance of Claudin-7 in Patients With Colorectal Cancer

High-Content Functional Screening of AEG-1 and AKR1C2 for the Promotion of Metastasis in Liver Cancer

AEG-1 Promotes Metastasis Through Downstream AKR1C2 and NF1 in Liver Cancer

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