HOXD3-overexpression increases integrin αvβ3 expression and deprives E-cadherin while it enhances cell motility in A549 cells

Ohta, Hiroya; Hamada, Jun Ichi; Tada, Mitsuhiro; Aoyama, Tetsuya; Furuuchi, Keiji; Takahashi, Yōko; Totsuka, Yasunori; Moriuchi, Tetsuya

doi:10.1007/s10585-006-9047-5

Cited by 32 publications

(29 citation statements)

References 35 publications

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“…Signal conduction mediated by syndecan-1 needs the cooperation of integrin β3 [34] . Mammary glandular epithelia short of syndecan-1 show rearrangement of integrin β3 and markedly low expression of E-cadherin at the same time [35] . Wound healing theory indicates that E-cadherin activates the migration of integrin β3-transfected cells and constrains them to separate from wound margin.…”

Section: Discussionmentioning

confidence: 99%

Relationship between cell adhesion molecules expression and the biological behavior of gastric carcinoma

Chu¹,

Ye²,

Tao³

et al. 2008

WJG

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analysis demonstrated that the mean survival time and 5-year survival rate were lower in the cases with low expressions of syndecan-1 and E-cadherin and high expression of integrin β3 (P < 0.01, in all cases). COX multivariate analysis showed that the expression level of syndecan-1 could be an independent prognostic index of gastric carcinoma (P < 0.01), whereas E-cadherin and integrin β3 could not be independent indexes (P > 0.05, P > 0.05 respectively). CONCLUSION:The low expression of syndecan-1 and E-cadherin and the high expression of integrin β3 are significantly correlated with the invasion and metastasis of gastric carcinoma, and they are highly correlated with each other. Therefore they may serve as important prognostic markers of gastric carcinoma. INTRODUCTIONGastric carcinoma is the most common malignant tumor of the digestive system. Two of the most important causes for the high mortality are invasion and metastasis. However, the mechanism of invasion and metastasis of gastric carcinoma is still not definitely clear at present [1] . Cell adhesion is one of the important steps in metastasis. Syndecan-1, E-cadherin and integrin β3 make up cell adhesion molecules (CAMs) and participate in the adhesion between the cell and the extracellular matrix [2] . Syndecan-1 is a set of transmembrane heparitin sulfate glycoproteins (HSPGS), which is present at the surface of most epithelia cells and take part in the adhesion between the cell and the extracellular matrix. The expression of syndecan-1 was augmented during epithelial regeneration and rearrangement in the stomach and other tissues [3,4] . E-cadherin is a calcium dependent intercellular Abstract AIM: To evaluate the relationship between the expression of cell adhesion molecules (CAMs) and the biological behavior of gastric carcinoma. METHODS:Expression of syndecan-1, E-cadherin and integrin β3 were evaluated by immunohistochemical study in a total of 118 gastric carcinomas and 20 nontumor gastric mucosas. RESULTS:T h e e x p r e s s i o n s o f s y n d e c a n -1 a n d E-cadherin were significantly lower in gastric carcinoma compared to non-tumor gastric mucosa, and the low expression rates were positively correlated to the tumor invasion depth, vessel invasion, lymph node metastasis and distant metastasis (P < 0.01 in all cases). However, the expression of integrin β3 was significantly higher in gastric carcinoma compared to non-tumor gastric mucosa, and the high expression rates were positively correlated to the tumor invasion depth, vessel invasion, lymph node metastasis and distant metastasis (P < 0.01 in all cases). In addition, the three protein expressions were correlated to the tumor growth pattern (P < 0.01, P < 0.01, and P < 0.05 respectively), but not correlated to tumor differentiation (P > 0.05, P > 0.05 and P > 0.05 respectively). Positive correlation was observed between the expressions of syndecan-1 and E-cadherin, but they which were negatively correlated to the expression of integrin β3 (P < 0.01 in all cases). Univariate

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Section: Discussionmentioning

confidence: 99%

Relationship between cell adhesion molecules expression and the biological behavior of gastric carcinoma

Chu¹,

Ye²,

Tao³

et al. 2008

WJG

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“…Because multiple cell types can be analyzed [9][10][11][12][13][14][15][16][17] , this method has the potential broad usage across multiple disciplines. The use of colloidal gold-coated glass coverslips allows for the measurement of a track area cleared by a moving cell.…”

Section: Discussionmentioning

confidence: 99%

“…With the use of freely available software, multiple tracks can be evaluated for each treatment to accomplish statistical requirements. The assay can be utilized to assess motility of many cell types, such as cancer cells 11,12 , fibroblasts 9 , neutrophils 13 , skeletal muscle cells 14 , keratinocytes 15 , trophoblasts 16 , endothelial cells 17 , and monocytes 10,[18][19][20][21][22] . The protocol involves the creation of slides coated with gold nanoparticles (Au°) that are generated by a reduction of chloroauric acid (Au 3+ ) by sodium citrate.…”

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confidence: 99%

A Quantitative Evaluation of Cell Migration by the Phagokinetic Track Motility Assay

Nogalski

Chan

Stevenson

et al. 2012

JoVE

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Cellular motility is an important biological process for both unicellular and multicellular organisms. It is essential for movement of unicellular organisms towards a source of nutrients or away from unsuitable conditions, as well as in multicellular organisms for tissue development, immune surveillance and wound healing, just to mention a few roles 1,2,3 . Deregulation of this process can lead to serious neurological, cardiovascular and immunological diseases, as well as exacerbated tumor formation and spread 4,5 . Molecularly, actin polymerization and receptor recycling have been shown to play important roles in creating cellular extensions (lamellipodia), that drive the forward movement of the cell 6,7,8 . However, many biological questions about cell migration remain unanswered.The central role for cellular motility in human health and disease underlines the importance of understanding the specific mechanisms involved in this process and makes accurate methods for evaluating cell motility particularly important. Microscopes are usually used to visualize the movement of cells. However, cells move rather slowly, making the quantitative measurement of cell migration a resource-consuming process requiring expensive cameras and software to create quantitative time-lapsed movies of motile cells. Therefore, the ability to perform a quantitative measurement of cell migration that is cost-effective, non-laborious, and that utilizes common laboratory equipment is a great need for many researchers.The phagokinetic track motility assay utilizes the ability of a moving cell to clear gold particles from its path to create a measurable track on a colloidal gold-coated glass coverslip 9,10 . With the use of freely available software, multiple tracks can be evaluated for each treatment to accomplish statistical requirements. The assay can be utilized to assess motility of many cell types, such as cancer cells 11,12 10,[18][19][20][21][22] . The protocol involves the creation of slides coated with gold nanoparticles (Au°) that are generated by a reduction of chloroauric acid (Au 3+ ) by sodium citrate. This method was developed by Turkevich et al. in 1951 23 and then improved in the 1970s by Frens et al. 24,25 . As a result of this chemical reduction step, gold particles (10-20 nm in diameter) precipitate from the reaction mixture and can be applied to glass coverslips, which are then ready for use in cellular migration analyses 9,26,27 . In general, the phagokinetic track motility assay is a quick, quantitative and easy measure of cellular motility. In addition, it can be utilized as a simple high-throughput assay, for use with cell types that are not amenable to time-lapsed imaging, as well as other uses depending on the needs of the researcher. Together, the ability to quantitatively measure cellular motility of multiple cell types without the need for expensive microscopes and software, along with the use of common laboratory equipment and chemicals, make the phagokinetic track motility assay a solid choice for sc...

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“…4a), but only efficiently increased We then tried to explore the underlying mechanism by investigating whether HoxD3, a transcription factor promoting avb3 expression [25], was required for the regulatory effect of NFjB. HoxD3 expression was not influenced by LPS and DTCMs (Fig.…”

Section: Tlr4 Signaling Increases Av and B3 Expressions In Metastaticmentioning

confidence: 99%

Triggering of Toll-like receptor 4 on metastatic breast cancer cells promotes αvβ3-mediated adhesion and invasive migration

Liao

Zhou

Yuan

et al. 2011

Breast Cancer Res Treat

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Triggering of Toll-like receptor 4 (TLR4) on tumor cells has been found to promote tumor progression by promoting tumor cell proliferation and survival. So far, however, the effect of TLR4 signaling on tumor metastasis has not been well elucidated. Here, we report that triggering of TLR4 on metastatic breast cancer cells could reciprocally regulate the expression of αvβ3 and the expressions of TPM1 and maspin, and promote αvβ3-mediated adhesion and invasive migration of the cells. In metastatic breast cancer cells, TLR4 signaling increased the expression of integrin αvβ3 by activating NF-κB, resulting in the increased adhesion capacity of tumor cells to the ligand for αvβ3, and the increased polymerization of actin and production of MMP-9 in tumor cells in response to ECM. HoxD3 was required for the up-regulation of αv and β3 expressions by NF-κB. Moreover, TLR4 signaling increased the expression of miR-21 in breast cancer cells by activating NF-κB. Accordingly, the expressions of TPM1 and maspin were decreased at protein level, whereas the transcription activity of these genes was not influenced. Consistent with the promoting effect on αvβ3-mediated adhesion and invasive migration, TLR4 signaling promoted the arrest of metastatic breast cancer cells in circulation and following invasion. The effect of TLR4 signaling could be abrogated by inhibiting NF-κB. These findings suggest that metastatic breast cancer cells could acquire higher metastatic potential due to triggering of TLR4 and activation of NF-κB in the cells, and that both TLR4 and NF-κB could be therapeutic targets for preventing metastasis of breast cancer cells.

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HOXD3-overexpression increases integrin αvβ3 expression and deprives E-cadherin while it enhances cell motility in A549 cells

Cited by 32 publications

References 35 publications

Relationship between cell adhesion molecules expression and the biological behavior of gastric carcinoma

Relationship between cell adhesion molecules expression and the biological behavior of gastric carcinoma

A Quantitative Evaluation of Cell Migration by the Phagokinetic Track Motility Assay

Triggering of Toll-like receptor 4 on metastatic breast cancer cells promotes αvβ3-mediated adhesion and invasive migration

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