Claudins upregulation in human colorectal cancer

Oliveira, Silvia Souza de; Oliveira, Ivanir Martins de; Souza, Wanderley de; Morgado‐Díaz, José Andrés

doi:10.1016/j.febslet.2005.09.091

Cited by 115 publications

(109 citation statements)

References 33 publications

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“…The expression of claudin-2 was also upregulated in lung adenocarcinoma cells (29), whereas claudin-7 was demonstrated to be downregulated in invasive ductal carcinomas of the breast (30). The expression of claudins-1, -3 and -4 was previously reported to be upregulated in human colorectal cancer (31). Furthermore, several studies have reported that the translocation of claudins is associated with tumor cell proliferation and survival (32,33).…”

Section: Introductionmentioning

confidence: 94%

Nuclear expression of claudin‑3 in human colorectal adenocarcinoma cell lines and tissues

et al. 2017

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Abstract.Claudins are members of a large family of transmembrane proteins, which are essential for the formation of tight junctions and have a significant effect on the biological behavior of tumor progression. Previous studies have demonstrated that several claudins show aberrant expression patterns in numerous types of cancer. The present study investigated the expression and localization of claudin-3 and claudin-7 in human colorectal adenocarcinoma cell lines and tissues. The protein expression levels of claudin-3 and claudin-7 were determined using immunocytochemical and immunohistochemical staining. Claudin-3, but not claudin-7, exhibited nuclear localization in the human colorectal adenocarcinoma Caco-2 and SW620 cell lines. Surgically resected colorectal adenocarcinoma tissue specimens were obtained, and the associations between the expression of claudin-3 or claudin-7 and various clinicopathological parameters were analyzed. The membranous expression rates of claudin-3 and claudin-7 were 58.0 and 50.0%, while their nuclear expression rates were 22.0 and 2.0%, respectively. The membranous expression of claudin-3 and claudin-7 was not associated with any clinicopathological factors, whereas the nuclear expression of claudin-3 was associated with histological type and was significantly increased in colorectal mucinous adenocarcinomas compared with that in well-to moderately-differentiated colorectal adenocarcinomas (P<0.01). However, no associations were observed between the nuclear expression of claudin-7 and any clinicopathological parameter. In conclusion, the nuclear expression of claudin-3 in colorectal mucinous adenocarcinoma may be involved in the biological transformation of tumors. The results from the present study indicated that claudin-3 is an important protein associated with histological type and has potential as a prognostic marker. Although the mechanisms underlying the nuclear localization of claudin-3 in tumorigenesis have not yet been elucidated in detail, the present results indicated the potential of claudin-3 as a histopathological biomarker for colorectal adenocarcinomas.

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Section: Introductionmentioning

confidence: 94%

Nuclear expression of claudin‑3 in human colorectal adenocarcinoma cell lines and tissues

et al. 2017

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“…Among these, the members of claudin family, which are transmembrane proteins with extracellular domains, interact with other claudins associated with adjacent cells for regulation of paracellular permeability [9,14]. Emerging evidence indicates that TJ disruption and dysregulation of TJ protein are early events in cancer cell invasion and metastasis [1,6,27,31]. These observations also indicate that claudins are dysregulated in many types of cancers and that the nature of the dysregulation is highly type-specific for given cancers.…”

Section: Discussionmentioning

confidence: 79%

“…Modulation of TJs, which are structures critical for maintenance of these functions in epithelial cells, in a number of epithelial cancers, including gastric adenocarcinoma, has been demonstrated [1,13,20,21,23]. Thus, TJ disruption and dysregulation of its composite proteins play critical roles in cancer progression, invasion, and metastasis, particularly epithelial cancers [6,27]. For example, Soler et al [24] first demonstrated that TER of colon carcinoma tissue was significantly lower than that of normal colon tissues but showed higher transepithelial paracellular permeability, which confirmed the loss of TJs.…”

Section: Discussionmentioning

confidence: 99%

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Inhibition of Cell Invasion by Ethyl Alcohol Extracts of Hizikia fusiforme in AGS Human Gastric Adenocarcinoma Cells

Choi

2010

Journal of Life Science

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In this study, we investigated the effects of ethyl alcohol extracts of Hizikia fusiforme (EHF) on the correlation between tightening of tight junctions (TJs) and anti-invasive activity in human gastric adenocarcinoma AGS cells. Inhibitory effects of EHF on cell proliferation, motility, and invasiveness were found to be associated with increased tightness of the TJs, which was demonstrated by an increase in transepithelial electrical resistance. Activities of matrix metalloprotease (MMP)-2 and -9 in AGS cells were dose-dependently inhibited by treatment with EHF, and this was also correlated with a decrease in expression of their mRNA and proteins; however, tissue inhibitor of metalloproteinase (TIMP)-1 and -2 mRNA levels were increased. Additionally, immunoblotting results indicated that EHF repressed the levels of claudin proteins (claudin-1, -3, and -4), major components of TJs that play key roles in control and selectivity of paracellular transport. Furthermore, EHF decreased expression of insulin such as growth factor-1 receptor proteins, while concurrently increasing that of thrombospondin-1 and E-cadherin. In conclusion, these results suggest that EHF treatment may inhibit tumor cell motility and invasion, and therefore act as a dietary source to decrease the risk of cancer metastasis.

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“…In partial contrast, reduced expression of Cldn4 and Cldn5 was detected in hepatocellular and renal carcinomas (Soini, 2005). In CRC, both, up-and down-regulation of claudin4 expression have been described (de Oliveira, et al, 2005, Ueda, et al, 2007, as well as aberrant expression of Cldn1. Another type of cell connection has been named cell-to-extracellular matrix (ECM) contacts.…”

Section: Introductionmentioning

confidence: 95%