The impact of CLAUDIN-1 on follicular thyroid carcinoma aggressiveness

Zwanziger, Denise; Badziong, Julia; Ting, Saskia; Moeller, Lars C.; Schmid, Kurt Werner; Siebolts, Udo; Wickenhauser, Claudia; Dralle, Henning; Fuehrer, Dagmar

doi:10.1530/erc-14-0502

Cited by 35 publications

(38 citation statements)

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“…Tzelepi et al demonstrated reduced expression of claudin-1, -4, and -7 in dedifferentiated thyroid carcinomas [14]. A recent study demonstrated that increased nuclear claudin-1 expression in FTC cell lines correlated with increased tumor cell motility, invasion, and metastasis which were potentially related to protein kinase C activity [9]. In the current cohort of 90 PTCs, no nuclear claudin-1 staining was noted in any tumors.…”

Section: Discussionmentioning

confidence: 41%

“…While several cellular mechanisms interacting with various players of cell signaling pathways regulate tumor cell invasiveness, altered expression of the tight junction integral molecules has been linked to the pathogenesis of malignant tumors. Claudins, which are one of the integral molecules of tight junctions maintaining the integrity of the cell polarity and barrier function, have also been linked to cell dysadhesion, increased cell motility, epithelial mesenchymal transition, cell proliferation as well as metastatic potential [6][7][8][9]. While one can except that downregulation of these molecules can result in loss of cell polarity and cell invasiveness, recent evidence suggests that both up and downregulation of claudins bear a biologic significance in a tumor-and claudin-specific manner [6][7][8][9].…”

Section: Discussionmentioning

confidence: 99%

“…Posttranscriptional modification of tight junction molecules including various claudins and occludin, and interaction of these molecules with other players of the cell signaling pathways have been an area of cancer research over the past years given their potential role in cancer initiation and progression [6][7][8][9]. Among various claudins, increased claudin-1 expression has been reported as a feature of PTC [10][11][12][13][14], whereas absence or weak expression is noted in non-tumorous thyroid parenchyma and some benign follicular epithelial-derived proliferations [10][11][12][13][14].…”

Section: Introductionmentioning

confidence: 99%

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The Value of HBME-1 and Claudin-1 Expression Profile in the Distinction of BRAF-Like and RAS-Like Phenotypes in Papillary Thyroid Carcinoma

et al. 2016

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This study compared the expression profile of HBME-1 and claudin-1 in 90 papillary thyroid carcinomas (PTCs) with respect to the tumor architecture and invasive growth as reflected in 46 BRAF-like, 31 non-invasive RAS, and 13 invasive RAS-like phenotypes. Individual tumors were given an expression score (max 300) by multiplying the percent positive tumor cells by the intensity score (range 0-3). The higher expression of HBME-1 and claudin-1 distinguished BRAF-like phenotype from RAS-like phenotype. The same correlation was also retained for both markers when comparing BRAF-like phenotype with non-invasive and invasive RAS-like phenotypes. The expression scores and positivity rates for both markers did not yield any statistical difference among BRAF-like PTCs. Except the higher positivity rate of HBME-1, invasive RAS-like tumors were not statistically different than their non-invasive counterparts with respect to the positivity rate of claudin-1 and the expression scores of both markers. A central lymph node dissection or selective lymph node sampling was available in 20 specimens. The absence of claudin-1 expression has not been a feature of lymph node metastasis in this series. Despite the limited number of nodal sampling, BRAF-like phenotype and claudin-1 positivity status have been considered the best determinants of positive predictive value and negative predictive value in the prediction of lymph node metastasis among variables, respectively. Adoption of the simplified architectural classification approach to PTCs showed distinct biomarker expression profile in this series; however, immunohistochemistry for HBME-1 and claudin-1 does not seem to be useful in the distinction of invasive RAS-like PTCs from their non-invasive counterparts. Given the overlapping molecular signatures within the RAS-like phenotype, further studies with additional biomarkers are still needed to identify distinct protein expression signatures of non-invasive RAS-like phenotype as this diagnostic category still remains a surgical diagnosis at this time.

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Section: Discussionmentioning

confidence: 41%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The Value of HBME-1 and Claudin-1 Expression Profile in the Distinction of BRAF-Like and RAS-Like Phenotypes in Papillary Thyroid Carcinoma

et al. 2016

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“…CLDN11 is a member of the claudin protein family and is a critical component of tight junctions, where it serves a key role in regulating cell junctions and cell adhesion (28). Previous results have indicated that CLDN11 may suppress the proliferation, invasion and apoptosis of many tumor types.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-421 promotes the proliferation and metastasis of gastric cancer cells by targeting claudin-11

Yang

Mei

Liu

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. The present study aimed to evaluate the expression of microRNA (miR)-421 in gastric cancer and to investigate its biological function and underlying mechanism of action in the development of gastric cancer. The expression of miR-421 was measured in 60 pairs of clinically removed gastric cancer tissues and matched adjacent normal gastric tissues by reverse transcription-quantitative polymerase chain reaction. In addition, following transfection with an miR-421 inhibitor to suppress the expression of miR-421, the proliferation, migration and cell cycle distribution of human gastric carcinoma MKN28/MKN74 cells were determined by cell counting, Transwell and flow cytometry assays. The target gene of miR-421 was also predicted using bioinformatic analysis and verified by dual-luciferase reporter gene assay and western blot analysis. Furthermore, overexpression of the miR-421 target protein was induced in MKN28/MKN74 cells to determine its function. It was observed that miR-421 was significantly upregulated in gastric cancer tissues and that the expression of miR-421 was associated with lymph node metastasis and the clinical stage of gastric cancer (all P<0.05). Claudin11 (CLDN11) was predicted and verified as a direct target of miR-421. In vitro experiments demonstrated that inhibition of miR-421 expression suppressed the proliferation and metastasis of MKN28/MKN74 cells and induced G1/S-phase cell cycle arrest (all P<0.05). Analagous results were observed in MKN28/MKN74 cells following overexpression of the CLDN11 protein. Collectively, these data suggest that miR-421 may promote the proliferation, invasion and metastasis of gastric cancer by inhibiting the expression of CLDN11.

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“…Although claudins are members of the tetraspanin family of proteins, which are integral to the structure and function of TJs, changes in the cellular localization of claudins serve an important role during tumorigenesis (19). Previous studies reported that the expression of claudin-1 increased in human colon cancers with mislocalization from the cell membrane to the nucleus and cytoplasm (19), the predominant cytoplasmic and nuclear localization of claudin-1 reduced apoptosis in nasopharyngeal carcinoma cells (28), and claudin-1 showed loss of membrane expression and increased nuclear localization in follicular thyroid carcinoma (39). The cytoplasmic expression of claudin-1 in metastatic melanoma cells was also shown to be critical for increased malignancy (27,40).…”

Section: Discussionmentioning

confidence: 99%

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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The impact of CLAUDIN-1 on follicular thyroid carcinoma aggressiveness

Cited by 35 publications

References 36 publications

The Value of HBME-1 and Claudin-1 Expression Profile in the Distinction of BRAF-Like and RAS-Like Phenotypes in Papillary Thyroid Carcinoma

The Value of HBME-1 and Claudin-1 Expression Profile in the Distinction of BRAF-Like and RAS-Like Phenotypes in Papillary Thyroid Carcinoma

MicroRNA-421 promotes the proliferation and metastasis of gastric cancer cells by targeting claudin-11

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

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