Differential Pattern of Integrin Receptor Expression in Differentiated and Anaplastic Thyroid Cancer Cell Lines

Hoffmann, Sebastian; Maschuw, Katja; Hassan, I.; Reckzeh, B; Wunderlich, Annette; Lingelbach, Susanne; Zielke, A.

doi:10.1089/thy.2005.15.1011

Cited by 26 publications

(19 citation statements)

References 42 publications

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“…Pilot studies to determine the degree of adhesion the cells demonstrated to different matrix proteins were performed using plates in which wells were coated with different matrix proteins including fibronectin, fibrinogen, laminin, Collagen I and IV (Cell Biolabs Inc., San Diego, CA). In concordance with the literature [31], HT29a cells were most adherent to collagen IV (three fold increase versus BSA control). Using collagen IV pre-coated 96 well plates (BD Biosciences, SanJose, CA), both clones of HT29a RCAN1HA cells displayed an enhanced cell adhesion to collagen IV in the presence of doxycycline in both cell lines.…”

Section: Resultssupporting

confidence: 91%

Regulator of calcineurin 1 modulates cancer cell migration in vitro

Espinosa

Shinohara

Porchia

et al. 2009

Clin Exp Metastasis

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Metastasis suppressors and other regulators of cell motility play an important role in tumor invasion and metastases. We previously identified that activation of the G protein coupled receptor 54 (GPR54) by the metastasis suppressor metastin inhibits cell migration in association with overexpression of Regulator of calcineurin 1 (RCAN1), an endogenous regulator of calcineurin. Calcineurin inhibitors also blocked cell migration in vitro and RCAN1 protein levels were reduced in nodal metastases in thyroid cancer. The purpose of the current study was to determine directly if RCAN1 functions as a motility suppressor in vitro. Several cancer cell lines derived from different cancer types with different motility rates were evaluated for RCAN1 expression levels. Using these systems we determined that reduction of endogenous RCAN1 using siRNA resulted in an increase in cancer cell motility while expression of exogenous RCAN1 reduced cell motility. In one cell line with a high migratory rate, the stability of exogenously expressed RCAN1 protein was reduced and was rescued by treatment with a proteasome inhibitor. Finally, overexpression of RCAN1 was associated with an increase in cell adhesion to collagen IV and reduced calcineurin activity. In summary, we have demonstrated that the expression of exogenous RCAN1 reduces migration and alters adhesion; and that the loss of endogenous RCAN1 leads to an increase in migration in the examined cancer cell lines. These results are consistent with a regulatory role for RCAN1 in cancer cell motility in vitro.

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Section: Resultssupporting

confidence: 91%

Regulator of calcineurin 1 modulates cancer cell migration in vitro

Espinosa

Shinohara

Porchia

et al. 2009

Clin Exp Metastasis

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“… 23 , 24 Hoffmann et al previously described integrin expression in several thyroid cancer cell lines including TPC1 cell line. 25 In contrast to their results, we observed a strong expression of both αvβ3 and αvβ5 in TPC1 cell line. In K1 and BCPAP cell lines, which were not investigated in Hoffmann’s study, the expression of αvβ3 and αvβ5 was modest as compared with that of TPC1 cells.…”

Section: Discussioncontrasting

confidence: 99%

The effect of antagonizing RGD-binding integrin activity in papillary thyroid cancer cell lines

Cheng¹,

Fěng²,

Ma³

et al. 2016

OTT

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Patients with papillary thyroid cancer (PTC) generally have good prognosis, but inoperable and radioactive iodine–refractory PTC still poses significant clinical challenges due to lack of effective treatment and higher mortality rates. Given the important role of integrins in multiple steps of tumor development, integrin-targeting therapy could be an effective strategy for PTC therapy. In this study, we investigated the antitumor effect of antagonizing Arg-Gly-Asp (RGD)-binding integrin activity in several PTC cell lines. Two RGD-binding integrin heterodimers αvβ3 and αvβ5 were first determined with fluorescence-activated cell sorting (FACS) and immunofluorescence assay. Cell proliferation and apoptosis were examined by Cell Counting Kit-8 assay and FACS, respectively. Cell migration and invasion were determined by transwell assays. All three PTC cell lines examined (BCPAP, K1, and TPC1) showed a moderate-to-high expression of αvβ3 and αvβ5 (P<0.05). Antagonizing the two heterodimers with the RGD-containing antagonist showed moderate inhibitory effect on cell viability of K1 and BCPAP cells, while the inhibitory effect was more significant in TPC1 cells. Similarly, the apoptotic effect induced by antagonizing αvβ3 and αvβ5 was much stronger in TPC1 cells than in BCPAP and K1 cells. Cell migration and invasion were significantly inhibited by αvβ3 and αvβ5 antagonism in all three PTC cell lines. Our results suggested that the demonstrated expression of RGD-binding integrin on PTC cells provides the possibility of integrin-targeting treatment in PTC. The strong apoptotic effect observed in TPC1 cells indicated that a subgroup of PTC patients may benefit from the cytotoxic effect of RGD-binding integrin antagonism, while the strong inhibitory effect on migration and invasion in all three PTC cells by antagonizing αvβ3 and αvβ5 showed there is an exciting possibility that targeting RGD-binding integrin may serve a potential therapeutic approach for metastatic PTC patients.

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“…In another study, Hoffmann and coworkers demonstrated a major differential expression pattern of integrin receptor molecules (IRM) in differentiated (FTC and PTC) and undifferentiated (ATC) thyroid cancer cell lines. Through cell substratum adhesion assays, they noted that the metastatic thyroid cancer cell lines express high levels of integrins α1-6 and β1 and show strong attachment to extracellular matrix (ECM) proteins including collagen I, collagen IV, laminin, and fibronectin (21). It is conceivable that these integrins may contribute to the development of metastatic disease.…”

Section: Discussionmentioning

confidence: 99%

Characterization of human follicular thyroid cancer cell lines in preclinical mouse models

Reeb

Ziegler

Lin

2016

Endocrine Connections

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Follicular thyroid cancer (FTC) is the second most common type of thyroid cancers. In order to develop more effective personalized therapies, it is necessary to thoroughly evaluate patient-derived cell lines in in vivo preclinical models before using them to test new, targeted therapies. This study evaluates the tumorigenic and metastatic potential of a panel of three human FTC cell lines (WRO, FTC-238, and TT1609-CO2) with defined genetic mutations in two in vivo murine models: an orthotopic thyroid cancer model to study tumor progression and a tail vein injection model to study metastasis. All cell lines developed tumors in the orthotopic model, with take rates of 100%. Notably, WRO-derived tumors grew two to four times faster than tumors arising from the FTC-238 and TT2609-CO2 cell lines. These results mirrored those of a tail vein injection model for lung metastasis: one hundred percent of mice injected with WRO cells in the tail vein exhibited aggressive growth of bilateral lung metastases within 35 days. In contrast, tail vein injection of FTC-238 or TT2609-CO2 cells did not result in lung metastasis. Together, our work demonstrates that these human FTC cell lines display highly varied tumorigenic and metastatic potential in vivo with WRO being the most aggressive cell line in both orthotopic and lung metastasis models. This information will be valuable when selecting cell lines for preclinical drug testing.

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Differential Pattern of Integrin Receptor Expression in Differentiated and Anaplastic Thyroid Cancer Cell Lines

Cited by 26 publications

References 42 publications

Regulator of calcineurin 1 modulates cancer cell migration in vitro

Regulator of calcineurin 1 modulates cancer cell migration in vitro

The effect of antagonizing RGD-binding integrin activity in papillary thyroid cancer cell lines

Characterization of human follicular thyroid cancer cell lines in preclinical mouse models

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