BACKGROUND： Stathmin is a ubiquitous cytosolic regulatory phosphoprotein and is overexpressed in different human malignancies. The main physiological function of stathmin is to interfere with microtubule dynamics by ...BACKGROUND： Stathmin is a ubiquitous cytosolic regulatory phosphoprotein and is overexpressed in different human malignancies. The main physiological function of stathmin is to interfere with microtubule dynamics by promoting depolymerization of microtubules or by preventing polymerization of tubulin heterodimers. Stathmin plays important roles in regulating many cellular functions as a result of its microtubuledestabilizing activity. Currently, the critical roles of stathmin in cancer cells, as well as in lymphocytes have been valued. This review discusses stathmin and microtubule dynamics in cancer development, and hypothesizes their possible relationship with epithelial-mesenchymal transition（EMT）.DATA SOURCES： A PubMed search using such terms as ＂stathmin＂, ＂microtubule dynamics＂, ＂epithelial-mesenchymal transition＂, ＂EMT＂, ＂malignant potential＂ and ＂cancer＂ was performed to identify relevant studies published in English.More than 100 related articles were reviewed.RESULTS： The literature clearly documented the relationship between stathmin and its microtubule-destabilizing activity of cancer development. However, the particular mechanism is poorly understood. Microtubule disruption is essential for EMT, which is a crucial process during cancer development. As a microtubule-destabilizing protein, stathmin may promote malignant potential in cancer cells by initiating EMT.CONCLUSIONS： We propose that there is a stathminmicrotubule dynamics-EMT（S-M-E） axis during cancer development. By this axis, stathmin together with itsmicrotubule-destabilizing activity contributes to EMT, which stimulates the malignant potential in cancer cells.展开更多
Background： Multiple sclerosis （MS） is a common central nervous system autoimmune disorder. Increasing number of genome-wide association study （GWAS） analyses hint that MS is strongly associated with genetics. Un...Background： Multiple sclerosis （MS） is a common central nervous system autoimmune disorder. Increasing number of genome-wide association study （GWAS） analyses hint that MS is strongly associated with genetics. Unfortunately, almost all the GWAS analyses were Caucasian population based. Numbers of risk loci might not be replicated in Chinese MS patients. Hence, we pertbrmed a MassArray Assay to genotype the previously reported variants located in the transcription regulation genes in order to elucidate their role in the Chinese MS patients. Methods： One hundred and forty-two relapsing-remitting MS （RRMS） patients and 301 healthy controls were consecutively collected from September 2, 2008, to June 7, 2013, as stage 1 subjects. Eight reported transcription regulation-related single-nucleotide polymorphisms （SNPs） were genotyped using the Sequenom MassArray system. In stage 2, another 44 RRMS patients and 200 healthy controls were consecutively collected and Sanger sequenced from April 7, 2015, to June 29, 2017, for the validation of positive results in stage 1. Differences in allele and genotype frequencies between patients and healthy controls, odds ratios, and 95% confidence intervals were calculated with the Chi-square test or Fisher＇s exact test. Hardy-Weinberg equilibrium was tested also using the Chi-square test. Results： In stage 1 analysis, we confirmed only one previously reported risk variant, rsl 1129295 in EOMES gene. We found that the frequency ofT/T genotype was much higher in MS group （χ2 = 10.251, P = 0.005） and the T allele ofrsl 1129295 increased the risk of MS （χ2 = 10.022, P = 0.002）. In stage 2 and combined analyses, the T allele of rsl 1129295 still increased the risk of MS （χ2 = 4.586, P- 0.030 and×2 = 16.378, P = 5.19×10 ^-5, respectively）. Conclusions： This study enhances the knowledge that the variant of EOMES is associated with increasing risk in Chinese RRMS patients and provides a potential therapeutic target in RRMS.展开更多
基金supported by grants from the National Natural Science Foundation of China(81172276,81001058,8110156,Sino-German GZ857)the Shanghai Committee of Science and Technology,China(11JC1402500)
文摘BACKGROUND： Stathmin is a ubiquitous cytosolic regulatory phosphoprotein and is overexpressed in different human malignancies. The main physiological function of stathmin is to interfere with microtubule dynamics by promoting depolymerization of microtubules or by preventing polymerization of tubulin heterodimers. Stathmin plays important roles in regulating many cellular functions as a result of its microtubuledestabilizing activity. Currently, the critical roles of stathmin in cancer cells, as well as in lymphocytes have been valued. This review discusses stathmin and microtubule dynamics in cancer development, and hypothesizes their possible relationship with epithelial-mesenchymal transition（EMT）.DATA SOURCES： A PubMed search using such terms as ＂stathmin＂, ＂microtubule dynamics＂, ＂epithelial-mesenchymal transition＂, ＂EMT＂, ＂malignant potential＂ and ＂cancer＂ was performed to identify relevant studies published in English.More than 100 related articles were reviewed.RESULTS： The literature clearly documented the relationship between stathmin and its microtubule-destabilizing activity of cancer development. However, the particular mechanism is poorly understood. Microtubule disruption is essential for EMT, which is a crucial process during cancer development. As a microtubule-destabilizing protein, stathmin may promote malignant potential in cancer cells by initiating EMT.CONCLUSIONS： We propose that there is a stathminmicrotubule dynamics-EMT（S-M-E） axis during cancer development. By this axis, stathmin together with itsmicrotubule-destabilizing activity contributes to EMT, which stimulates the malignant potential in cancer cells.
基金This study was supported by the grants from the National Natural Science Foundation of China （No. 81371414 and No. 81125009）.
文摘Background： Multiple sclerosis （MS） is a common central nervous system autoimmune disorder. Increasing number of genome-wide association study （GWAS） analyses hint that MS is strongly associated with genetics. Unfortunately, almost all the GWAS analyses were Caucasian population based. Numbers of risk loci might not be replicated in Chinese MS patients. Hence, we pertbrmed a MassArray Assay to genotype the previously reported variants located in the transcription regulation genes in order to elucidate their role in the Chinese MS patients. Methods： One hundred and forty-two relapsing-remitting MS （RRMS） patients and 301 healthy controls were consecutively collected from September 2, 2008, to June 7, 2013, as stage 1 subjects. Eight reported transcription regulation-related single-nucleotide polymorphisms （SNPs） were genotyped using the Sequenom MassArray system. In stage 2, another 44 RRMS patients and 200 healthy controls were consecutively collected and Sanger sequenced from April 7, 2015, to June 29, 2017, for the validation of positive results in stage 1. Differences in allele and genotype frequencies between patients and healthy controls, odds ratios, and 95% confidence intervals were calculated with the Chi-square test or Fisher＇s exact test. Hardy-Weinberg equilibrium was tested also using the Chi-square test. Results： In stage 1 analysis, we confirmed only one previously reported risk variant, rsl 1129295 in EOMES gene. We found that the frequency ofT/T genotype was much higher in MS group （χ2 = 10.251, P = 0.005） and the T allele ofrsl 1129295 increased the risk of MS （χ2 = 10.022, P = 0.002）. In stage 2 and combined analyses, the T allele of rsl 1129295 still increased the risk of MS （χ2 = 4.586, P- 0.030 and×2 = 16.378, P = 5.19×10 ^-5, respectively）. Conclusions： This study enhances the knowledge that the variant of EOMES is associated with increasing risk in Chinese RRMS patients and provides a potential therapeutic target in RRMS.
