Clinical significance of expression of fibrous sheath interacting protein 1 in colon cancer

BACKGROUND The occurrence and development of colon cancer are complex,involving a variety of genetic changes,such as mutation and activation of oncogenes,inactivation of tumour suppressor genes,and aberrant proliferation and apoptosis regulation mechanisms.Fibrous sheath interacting protein 1(FSIP1)is a newly discovered oncogene that is frequently activated in a variety of tumours such as breast cancer and bladder cancer.However,the clinical significance of FSIP1 in colon cancer is unclear.In this study,we analysed the clinical significance of expression of FSIP1 in human colon cancer,aimed to clarify the biological role of FSIP1 in the development and progression of colon cancer.AIM To investigate the clinical significance of expression of FSIP1 in colon cancer.METHODS From March 2011 to March 2014,302 specimens of tumour tissues and paracancerous tissues were obtained from patients pathologically diagnosed with colon cancer at Shengjing Hospital of China Medical University.Immunohistochemistry was used to detect FSIP1 expression in colon cancer tissues and adjacent normal tissues.Spearman correlation coefficient and Cox regression analyses were used to determine the relationship between FSIP1 expression and clinicopathological factors and prognosis,as well as the impact on survival.RESULTS Compared with its expression in adjacent normal tissues,FSIP1 was expressed at higher levels in colon cancer tissues.Spearman correlation analysis showed that high expression of FSIP1 was positively correlated with clinicopathological stage,lymph node metastasis,and poor prognosis in colon cancer;it was negativel correlated with the degree of tumour differentiation.Cox regression analysis showed that high FSIP1 expression was an independent risk factor for the prognosis of colon cancer patients.CONCLUSION High expression of FSIP1 may be one of the important factors affecting the clinical outcome of colon cancer patients and leading to poor prognosis.

Müller cells are activated in response to retinal outer nuclear layer degeneration in rats subjected to simulated weightlessness conditions

A microgravity environment has been shown to cause ocular damage and affect visual acuity,but the underlying mechanisms remain unclear.Therefore,we established an animal model of weightlessness via tail suspension to examine the pathological changes and molecular mechanisms of retinal damage under microgravity.After 4 weeks of tail suspension,there were no notable alterations in retinal function and morphology,while after 8 weeks of tail suspension,significant reductions in retinal function were observed,and the outer nuclear layer was thinner,with abundant apoptotic cells.To investigate the mechanism underlying the degenerative changes that occurred in the outer nuclear layer of the retina,proteomics was used to analyze differentially expressed proteins in rat retinas after 8 weeks of tail suspension.The results showed that the expression levels of fibroblast growth factor 2(also known as basic fibroblast growth factor)and glial fibrillary acidic protein,which are closely related to Müller cell activation,were significantly upregulated.In addition,Müller cell regeneration and Müller cell gliosis were observed after 4 and 8 weeks,respectively,of simulated weightlessness.These findings indicate that Müller cells play an important regulatory role in retinal outer nuclear layer degeneration during weightlessness.