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The mechanical signals within the extracellular matrix (ECM) regulate cell growth, proliferation and differentiation, and integrins function as the hub between the ECM and cellular actin. Focal adhesions (FAs) are multi‑protein, integrin‑containing complexes, acting as tension‑sensing anchoring points that bond cells to the extracellular microenvironment. Talin‑1 serves as the central protein of FAs that participates in the activation of integrins and connects them with the actin cytoskeleton. As a cytoplasmic protein, Talin‑1 consists of a globular head domain and a long rod comprised of a series of α‑helical bundles. The unique structure of the Talin‑1 rod domain permits folding and unfolding in response to the mechanical stress, revealing various binding sites. Thus, conformation changes of the Talin‑1 rod domain enable the cell to convert mechanical signals into chemical through multiple signaling pathways. The present review discusses the binding partners of Talin‑1, their interactions, effects on the cellular processes, and their possible roles in diseases.Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that the Transwell cell migration assay data shown in Figs. 3B and 9B were strikingly similar to data appearing in different form in other articles by different authors. Owing to the fact that the contentious data in the above article had already been published elsewhere, or were already under consideration for publication, prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. After having been in contact with the authors, they agreed with the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 18 5603‑5613, 2018; DOI 10.3892/mmr.2018.9572].Bone is continuously remodeled in a dynamic process maintained by osteoclasts and osteoblasts, and imbalances in the relative activities of these cell types can cause various pathological conditions, including rheumatoid arthritis and osteoporosis. Osteoclasts are multinucleated cells that serve an important role in regulating the development of osteoporosis. Furthermore, P2X7 receptor activation has a vital role in physiological and pathological reactions in bone, including bone disease. Therefore, the present study aimed to investigate the effect of P2X7 receptor on osteoclast differentiation and to explore the underlying molecular mechanism by western blotting and tartrate‑resistant acid phosphatase staining. The results indicated that the expression levels of P2X7 receptor and intracellular Ca2+ concentration levels were very high in mature osteoclasts. Furthermore, P2X7 receptor overexpression increased the number of multinucleated osteoclasts and the expression of osteoclastogenesis‑related proteins. P2X7 receptor overexpression was also associated with downstream activation of Ca2+/calcineurin/nuclear factor of activated T cells c1 (NFATc1) signaling and increased expression of autophagy‑related proteins during osteoclast differentiation. By contrast, knockdown of P2X7 receptor exerted the opposite effects. Notably, FK506 (a Ca2+/calcineurin/NFATc1 signaling inhibitor) abrogated P2X7 receptor overexpression‑induced osteoclast differentiation and activation of autophagy. Moreover, 3‑MA (an autophagy inhibitor) significantly suppressed P2X7 receptor overexpression‑induced osteoclast differentiation. In conclusion, P2X7 receptor knockdown may suppress osteoclast differentiation by modulating autophagy and the Ca2+/calcineurin/NFATc1 signaling pathway.Yin Yang 1 (YY1) is a multifunctional transcription factor with critical roles in carcinogenesis and metastasis. However, its biological role and clinical impact in colorectal cancer (CRC) remain unclear. In the present study, the function and underlying molecular mechanisms of YY1 in CRC progression were investigated. The immunohistochemistry (IHC) of 143 CRC tissues revealed a significant correlation of low YY1 expression with aggressive clinicopathological features, increased metastasis and recurrence and poor patient survival. Multivariate analysis identified low YY1 expression as an independent poor prognostic factor. Subsequently, the IHC of 66 paired CRC primary tumor and liver metastasis tissues revealed that low YY1 expression in the primary CRC was significantly associated with multiple liver metastases, major hepatectomy, extrahepatic metastasis and poor prognosis. In vitro experiments revealed that YY1 knockdown promoted the migration and invasion of CRC cells. To examine the downstream genes of YY1, a cDNA microarray assay was conducted and the differentially expressed genes between the YY1‑knockdown and control cells were compared. Integrin alpha V (ITGAV) and integrin beta 1 (ITGB1) were identified as upregulated hub genes using gene enrichment analysis and protein‑protein interaction analyses. Western blotting and IHC confirmed YY1 expression to be negatively correlated with ITGAV and ITGB1 expression. In summary, it was revealed that YY1, as a tumor‑suppressor in CRC, contributes to the survival of patients with CRC. Low YY1 expression was associated with the poor prognosis of the patients with primary CRC and liver metastases. YY1 suppressed the expression of ITGAV and ITGB1, and this transcriptional regulation may lead to the suppression of CRC cell migration and invasion.Osteoprotegerin (OPG) is a negative regulator of osteoclast formation by competing with receptor activator of the nuclear factor-κB (NF-κB) ligand (RANKL) for RANK. OPG is not only a soluble decoy receptor for RANKL, but is also considered as a direct effector of osteoclast functions. However, the mechanismsresponsible for OPG-induced changes to osteoclast bone resorption functionsremain unknown. P2X7R is involved in the process of multinucleation and cell fusion. Therefore, in the present study, mitogen-activated protein kinase (MAPK) inhibitors and the RNA interference of purinergic receptor P2X7 (P2X7R) were usedtoexamine the effects of P2X7R-mediated MAPK signaling on changes to osteoclast adhesion structure induced by OPG; for this purpose, western blot analysis and immunofluorescence staining were performed. The results revealed that OPG inhibited osteoclast adhesion-related protein expression, disrupted adhesion protein distribution, and destroyed osteoclast filopodia and lamellipodia structures. The inhibitors partially restored osteoclast adhesion structure, including protein expression, distribution and cell morphology. The absence of P2X7R markedly inhibited osteoclast formation, and subsequent OPG treatment accelerated the damage to adhesion structures. However, P2X7R activation significantly recosvered the phosphorylation of paxillin, vinculin, phosphorylated protein tyrosine kinase 2 and SRC proto-oncogene, non-receptor tyrosine kinase induced by OPG, and their distribution was uniform at the osteoclast periphery. P2X7R silencing suppressed the phosphorylation of MAPK. On the whole, the findings of the present study highlighta key role of P2X7R/MAPK signaling in osteoclast adhesion, and provide a novel therapeutic target for bone disease.Head and neck cancers are diverse and complex diseases characterised by unregulated growth of tumour cells in various parts of the head and neck region, such as in the buccal mucosa, floor of the mouth, tongue, oropharynx, hypopharynx, oesophagus, nasopharynx and salivary glands. Partial or total glossectomy, radiation or chemotherapy greatly affect patient quality of life. However, even following treatment, patients may relapse. Nicotine‑derived nitrosamines and alcohol are the major etiological factors underlying this deadly disease. Deutivacaftor These compounds induce DNA damage that may lead to mutation in crucial genes, such as p53 and p21, which are important to regulate cell proliferation, thus leading to cancer. CD9 is a tetraspanin, which are a group of transmembrane proteins that have a role in cell motility and adhesion. The present review aimed to explore the role of CD9 in head and neck cancer. Epidermal growth factor receptor activity and cell proliferation are regulated by the CD9‑integrin/CD9‑transforming growth factor interaction. Hence, CD9 can play a dual role in various types of cancer.Clear cell renal cell carcinoma (ccRCC) is the most common and aggressive subtype of kidney cancer, with high mortality rates worldwide. The sonic hedgehog (SHH) molecular cascade is altered in various malignancies in tumorigenesis, and several SHH pathway inhibitors have been considered as potential anticancer drugs. The aim of the present study was to determine the expression profile of SHH signaling components and their target genes in ccRCC. Additionally, the present study examined the effects of SHH pathway inhibitory drugs (RU‑SKI43, cyclopamine and GLI‑antagonist 61) on cell viability, cell cycle progression, expression levels of SHH target genes and migration ability in 786‑O, ACHN and HK2 cells. The study also included paired tumor and normal samples from 62 patients with ccRCC. The mRNA levels in clinical samples and cell lines were measured via reverse transcription‑quantitative PCR. Cell viability was examined using a sulforhodamine B assay. Flow cytometry was used to investigate cell cycle progrestudy suggested that SHH signaling may be involved in the early development of ccRCC, and the expression levels of CCND1 and VEGFA may serve as prognostic factors of this disease. Cyclopamine and RU‑SKI43 appear to be potential anti‑renal cell carcinoma drugs; however, this hypothesis requires verification by further in vivo studies.
To investigate how next of kin of persons with spinal cord injury (SCI) experience various life areas in terms of caregiving, participation, and quality of life, and the impact of personal characteristics of next of kin and SCI characteristics.

Survey of next of kin linked to data on persons with SCI in the Norwegian SCI Registry.

A total of 73 next of kin identified by persons with SCI.

Outcome measures were caregiving (4 measures), participation (1 measure), and quality of life (2 measures).

Participants (73% partners, 73% female, mean age 56.4 years) gave various support to the person with SCI and considered it important to care and were happy to do so. Three-quarters of participants reported good mental health and life satisfaction, while one-quarter reported high levels of caregiver strain, especially related to emotional adjustments. Higher levels of caregiver strain were reported by participants of working age (< 67 years), and by those with middle level education.

The majority of next of kin of persons living with SCI in Norway are doing well in most life areas. Caregiver strain may be reduced by strengthening the ability of next of kin to cope with emotional challenges.
The majority of next of kin of persons living with SCI in Norway are doing well in most life areas. Caregiver strain may be reduced by strengthening the ability of next of kin to cope with emotional challenges.
To investigate whether blood flow restricted walking exercise is feasible in patients with knee osteoarthritis, and to examine changes in functional performance and self-reported function.

Feasibility study.

Fourteen elderly individuals diagnosed with knee osteoarthritis participated in 8-10 weeks of outdoor walking (4 km/h, 20 min/session, 4 times/week) with partial blood flow restriction applied to the affected leg. Adherence, dropouts and adverse events were registered. Timed Up and Go test, 30-s sit-to-stand performance, 40-m fast-paced walk speed, stair-climbing and Knee Osteoarthritis Outcome Score were assessed pre- and post-training.

Nine participants completed the intervention, while 5 participants withdrew (4 due to intervention-related reasons). In non-completing participants baseline body mass index (BMI) (p = 0.05) and knee pain (p = 0.06) were higher, while gait performance (p = 0.04) was lower. Considering completed case data, the training-adherence rate was 93%, while mean knee pain in the affected leg was 0.
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