OBJECTIVETo evaluate the chemical composition of the modified surface of fluoride ion-implanted titanium and assess the effect on the formation of focal adhesion plaque in vitro.

METHODSPure commercial titanium discs were treated with fluoride ion implantation by plasma immersion ion implantation technique (PIII) and chemical composition and value of the surface modification layer were characterized by X-ray photoelectron spectrometer (XPS). In order to investigate the formation of focal adhesion plaque, MG-63 cells were seeded onto the surfaces of the modified Ti discs and quantified by morphometric analysis using an immunofluorescence microscope.

RESULTSThe full range XPS spectra and fitting results indicated that the surface of fluoride ion-implanted titanium was the mixture of titanium dioxide and titanium trifluoride. Meanwhile, the quantity of focal adhesion plaque on fluoride ion-implanted titanium was more than that on the non-implanted titanium after 6 hours' cell culture.

CONCLUSIONThe XPS data revealed that the modified surface layer of fluoride ion-implanted titanium contained titanium dioxide and titanium trifluoride, which could enhance the formation of focal adhesion plaque.

Integrins are a large family of heterodimeric cell adhesion molecules composed of α and β subunits. Through interaction with their specific ligands, integrins mediate cell-cell and cell-extracellular matrix interactions. Via outside-in signaling, integrins can recruit cytoplasmic proteins to their intracellular domains and then cluster into supramolecular structures and trigger downstream signaling. Integrin activation is associated with a global conformation rearrangement from bent to extended in ectodomains and the separation of α and β subunit cytoplasmic domains. During cell migration, integrins regulate the focal adhesion dynamics and transmit forces between the extracellular matrix and the cell cytoskeleton. In tumor microenvironment, integrins on multiple kinds of cells could be activated, which modulates cell migration into tumor and contributes to angiogenesis and tumor metastasis. Here, we review the mechanism of integrin activation, dynamics of focal adhesions during cell migration and tumor metastasis.
Cell Adhesion ; Cell Adhesion Molecules ; Focal Adhesions ; Integrins ; Signal Transduction

PURPOSE: To evaluate the postoperative outcome of the multiple slit on plaque plication technique for the treatment of Peyronie's disease. MATERIALS AND METHODS: We retrospectively evaluated 22 patients who underwent plaque incision with penile plication for the surgical treatment of Peyronie's disease, who had failed medical treatment between 2009 and 2014. Patients were grouped by preoperative degree of penile curvature into Group I: mild (n=5, 22.7%), Group II: moderate (n=11, 50.0%), and Group III: severe (n=6, 27.3%). After a thorough review of the medical records, we evaluated (a) the correction of the curvature; (b) sexual function; and (c) any penile shortening or other complications. RESULTS: The mean postoperative follow-up period was 39 months. Complete correction of the curvature was attained in 21 patients (95.5%). As an inevitable complication, minimal penile shortening (<1.5 cm) was reported by 14 patients (82.4%) but did not adversely affect sexual intercourse (0%), and all patients found the extent of penile shortening to be acceptable. Nineteen patients had good erectile function (International Index of Erectile Function >21). The most frequent complication was subcutaneous penile edema in three patients (13.6%), which was resolved within about 3 months following surgery. CONCLUSIONS: As a modified technique, multiple slit on plaque with plication is a simple, minimally-invasive and effective technique for correcting penile curvature regardless of curvature severity. The degree of penile curvature does not significantly predict the amount of penile length loss.
Coitus ; Edema ; Focal Adhesions ; Follow-Up Studies ; Humans ; Male ; Medical Records ; Penile Induration* ; Retrospective Studies

Due to the polygenic nature of cancer, it is believed that breast cancer is caused by the perturbation of multiple genes and their complex interactions, which contribute to the wide aspects of disease phenotypes. A systems biology approach for the identification of subnetworks of interconnected genes as functional modules is required to understand the complex nature of diseases such as breast cancer. In this study, we apply a 3-step strategy for the interpretation of microarray data, focusing on identifying significantly perturbed metabolic pathways rather than analyzing a large amount of overexpressed and underexpressed individual genes. The selected pathways are considered to be dysregulated functional modules that putatively contribute to the progression of disease. The subnetwork of protein-protein interactions for these dysregulated pathways are constructed for further detailed analysis. We evaluated the method by analyzing microarray datasets of breast cancer tissues; i.e., normal and invasive breast cancer tissues. Using the strategy of microarray analysis, we selected several significantly perturbed pathways that are implicated in the regulation of progression of breast cancers, including the extracellular matrix-receptor interaction pathway and the focal adhesion pathway. Moreover, these selected pathways include several known breast cancer-related genes. It is concluded from this study that the present strategy is capable of selecting interesting perturbed pathways that putatively play a role in the progression of breast cancer and provides an improved interpretability of networks of protein-protein interactions.
Breast ; Breast Neoplasms ; Focal Adhesions ; Metabolic Networks and Pathways ; Microarray Analysis ; Phenotype ; Statistics as Topic ; Systems Biology

The biophysical properties of the extracellular matrix (ECM) dictate tissue-specific cell behaviour. In the skeleton system, bone shows the potential to adapt its architecture and contexture to environmental rigidity via the bone remodelling process, which involves chondrocytes, osteoblasts, osteoclasts, osteocytes and even peripheral bone marrow-derived stem/stromal cells (BMSCs). In the current study, we generated stiff (~1 014 ± 56) kPa, Young's modulus) and soft (~46 ± 11) kPa silicon-based elastomer polydimethylsiloxane (PDMS) substrates by mixing curing agent into oligomeric base at 1:5 and 1:45 ratios, respectively, and investigated the influence of substrate stiffness on the cell behaviours by characterizing cell spreading area, cell cytoskeleton and cell adhesion capacity. The results showed that the cell spreading areas of chondrocytes, osteoblasts, osteoclasts, osteocytes and BMSCs were all reduced in the soft substrate relative to those in the stiff substrate. F-actin staining confirmed that the cytoskeleton was also changed in the soft group compared to that in the stiff group. Vinculin in focal adhesion plaques was significantly decreased in response to soft substrate compared to stiff substrate. This study establishes the potential correlation between microenvironmental mechanics and the skeletal system, and the results regarding changes in cell spreading area, cytoskeleton and cell adhesion further indicate the important role of biomechanics in the cell-matrix interaction.
Actins ; Cell Adhesion ; Elastic Modulus ; Focal Adhesions ; physiology ; Humans ; Vinculin ; analysis ; metabolism

BACKGROUND: Cortactin and focal adhesion kinase (FAK) are two important components among actin cross-linking proteins that play a central role in cell migration. METHODS: The aims of this study were to evaluate the expression of cortactin and FAK in normal colorectal mucosa and colorectal adenocarcinoma (CRC) using tissue microarray of 2 mm cores to correlate their expression with other clinicopathological factors and, investigate their prognostic significance. RESULTS: Twenty (9%) and 24 cases (11%) of normal colorectal mucosa were immunoreactive for cortactin and FAK. In addition, 184 (84%) and 133 cases (61%) of CRCs were immunoreactive for cortactin and FAK, respectively. Cortactin expression was associated with histologic differentiation and FAK expression. Cortactin, but not FAK expression was also correlated with poor overall and relapse-free survival and served well as an independent prognostic factor for poor survival. CONCLUSIONS: Cortactin expression, in association with FAK expression, may plays an important role in tumor progression. Furthermore, it may also be a satisfactory biomarker to predict tumor progression and survival in CRC patients.
Actins ; Adenocarcinoma ; Calcium Hydroxide ; Colorectal Neoplasms ; Cortactin ; Focal Adhesion Protein-Tyrosine Kinases ; Focal Adhesions ; Humans ; Immunohistochemistry ; Mucous Membrane ; Proteins ; Zinc Oxide

Resistance to the induction of apoptosis is a possible mechanism by which tumor cells can survive anti-neoplastic treatments. Melanoma is notoriously resistant to anti-neoplastic therapy. Previous studies have demonstrated focal adhesion kinase (FAK) overexpression in melanoma cell lines. Given its probable role in mediating resistance to apoptosis, many researchers have sought to determine whether the downregulation of FAK in melanoma cells would confer a greater sensitivity to anti-neoplastic agents. Genistein is a known inhibitor of protein-tyrosine kinase (PTK), which may attenuate the growth of cancer cells by inhibiting the PTK-mediated signaling pathway. This present study was undertaken to investigate the effect of genistein on the expression of FAK and cell cycle related proteins in the G361 melanoma cell line. Genistein was found to have a preferential cytotoxic effect on G361 melanoma cells over HaCaT normal keratinocytes. Genistein decreased the expression of 125 kDa phosphotyrosine kinase and the FAK protein in particular. Genistein treatment did not affect the expression of p53 in G361 cells in which p21 is upregulated. The expression of cyclin B and cdc2 was downregulated by genistein treatment. Taken together, our data indicate that genistein induces the decreased proliferation of G361 melanoma cells via the inhibition of FAK expression and regulation of cell cycle genes. This suggests that the use of genistein may be a viable approach to future melanoma treatments.
Apoptosis ; Cell Cycle ; Cell Line ; Cyclin B ; Down-Regulation ; Focal Adhesion Protein-Tyrosine Kinases ; Focal Adhesions ; Genes, cdc ; Genistein ; Keratinocytes ; Melanoma ; Negotiating ; Phosphotransferases ; Phosphotyrosine ; Protein-Tyrosine Kinases ; Proteins

OBJECTIVE: E-cadherin/catenin adhesion complex is fundamentally involved in epithelial cancer invasion and metastasis. Focal adhesion kinase (FAK) is one of the molecules that may be involved in the regulation of focal adhesion integrity and the progression of cancer to invasion and metastasis. The present study was aimed to explore that the beta- & alpha-catenin might be involved in the invasion and metastasis of cervical carcinoma, and their expression might be related with other clinicopathologic factors or associated with FAK in cervical cancer. METHODS: The tissues were obtained from the 26 patients with cervical carcinoma and the 9 patients with normal cervix undergoing hysterectomy. The proteins were extracted and the expression of beta- and alpha- catenin and FAK were studied with a western blot analysis. The coexpression of alpha-catenin and FAK was examined with an immunoprecipitation. The clinicopathologic factors were reviewed with the charts of patients and the results were analysed with the Chi-square test and Spearman's correlation test. RESULTS: The expression of beta- and alpha-catenin in cervical carcinoma was lower than that in normal cervix (p<0.05). Their expression was not correlated with other clinicopathologic factors. The expression of FAK in cervical carcinoma was related with the expression of alpha-catenin. CONCLUSION: This study showed that the expression of beta- & alpha-catenin is involved in the invasion of cervical carcinoma and the FAK expression might be associated with the alpha-catenin expression in cervical carcinoma.
alpha Catenin* ; Blotting, Western ; Cervix Uteri ; Chi-Square Distribution ; Female ; Focal Adhesion Protein-Tyrosine Kinases* ; Focal Adhesions* ; Humans ; Hysterectomy ; Immunoprecipitation ; Neoplasm Metastasis ; Uterine Cervical Neoplasms

OBJECTIVE: E-cadherin/catenin adhesion complex is fundamentally involved in epithelial cancer invasion and metastasis. Focal adhesion kinase (FAK) is one of the molecules that may be involved in the regulation of focal adhesion integrity and the progression of cancer to invasion and metastasis. The present study was aimed to explore that the beta- & alpha-catenin might be involved in the invasion and metastasis of cervical carcinoma, and their expression might be related with other clinicopathologic factors or associated with FAK in cervical cancer. METHODS: The tissues were obtained from the 26 patients with cervical carcinoma and the 9 patients with normal cervix undergoing hysterectomy. The proteins were extracted and the expression of beta- and alpha- catenin and FAK were studied with a western blot analysis. The coexpression of alpha-catenin and FAK was examined with an immunoprecipitation. The clinicopathologic factors were reviewed with the charts of patients and the results were analysed with the Chi-square test and Spearman's correlation test. RESULTS: The expression of beta- and alpha-catenin in cervical carcinoma was lower than that in normal cervix (p<0.05). Their expression was not correlated with other clinicopathologic factors. The expression of FAK in cervical carcinoma was related with the expression of alpha-catenin. CONCLUSION: This study showed that the expression of beta- & alpha-catenin is involved in the invasion of cervical carcinoma and the FAK expression might be associated with the alpha-catenin expression in cervical carcinoma.
alpha Catenin* ; Blotting, Western ; Cervix Uteri ; Chi-Square Distribution ; Female ; Focal Adhesion Protein-Tyrosine Kinases* ; Focal Adhesions* ; Humans ; Hysterectomy ; Immunoprecipitation ; Neoplasm Metastasis ; Uterine Cervical Neoplasms

PURPOSE: In the pathogenesis of proliferative vitreoretinopathy (PVR), retinal pigment epithelial (RPE) cells do not undergo apoptosis after separation from the basement membrane. In order to investigate the mechanism by which RPE cells resist apoptosis in PVR, the expression of focal adhesion kinase after cryotherapy was studied. METHODS: After lensectomy and vitrectomy was performed on rabbit eyes, a retinal tear was created. Cryotherapy was applied to the tear site one week after the tear creation. Rabbits were sacrificed at 1, 4 and 7 days after the tear formation and 30 minutes, 1, 4, 7, 9, 21 days after cryotherapy. Eyes were stained with anti-focal adhesion kinase (FAK) antibody. RESULTS: Expression of FAK increased after the tear formation and remained increased until 21days after cryotherapy. CONCLUSIONS: These data show that creation of a retinal tear and cryotherapy increases FAK expression and may contribute to resistance to apoptosis.
Apoptosis ; Basement Membrane ; Cryotherapy* ; Epithelial Cells* ; Focal Adhesion Protein-Tyrosine Kinases* ; Focal Adhesions* ; Phosphotransferases ; Rabbits ; Retinal Perforations ; Retinaldehyde* ; Vitrectomy ; Vitreoretinopathy, Proliferative