BACKGROUND:With the increase of age,the function of bone marrow-derived mesenchymal stem cells is gradually reduced,and delaying the aging of bone marrow-derived mesenchymal stem cells itself has become an important topic.OBJECTIVE:To explore ways to delay the aging of bone marrow-derived mesenchymal stem cells by changing the expression of telomerase Cajal body protein 1(TCAB1)gene.METHODS:Mouse bone marrow-derived mesenchymal stem cells were cultured by cell adhesion method.TCAB1 gene in bone marrow-derived mesenchymal stem cells was overexpressed and interfered by recombinant lentivirus technique.The expression of aging related genes P16,P21,P53,and P27 was detected by qPCR.The relative length of telomeres was detected by qPCR.The expression of aging proteins P16,P21,P53,and P27 was detected by western blot assay.Cell proliferation was detected by CCK-8 assay.Annexin V-PE/7-AAD apoptosis kit was used to detect the degree of cell apoptosis.RESULTS AND CONCLUSION:Bone marrow-derived mesenchymal stem cell lines overexpressing TCAB1 gene had decreased expression of senescence related genes and proteins,increased Telomere relative length,stronger cell proliferation,less apoptosis,and a youthful state.The expression of age-related genes and proteins in bone marrow mesenchymal stem cells interfering with TCAB1 gene increased,and the relative telomere length decreased;cell proliferation ability was weak;cell apoptosis was more,and cells showed senescence.These results indicate that increasing the expression of TCAB1 in an appropriate range can delay the rate of cell senescence.

BACKGROUND:With the increase of age,the function of bone marrow-derived mesenchymal stem cells is gradually reduced,and delaying the aging of bone marrow-derived mesenchymal stem cells itself has become an important topic.OBJECTIVE:To explore ways to delay the aging of bone marrow-derived mesenchymal stem cells by changing the expression of telomerase Cajal body protein 1(TCAB1)gene.METHODS:Mouse bone marrow-derived mesenchymal stem cells were cultured by cell adhesion method.TCAB1 gene in bone marrow-derived mesenchymal stem cells was overexpressed and interfered by recombinant lentivirus technique.The expression of aging related genes P16,P21,P53,and P27 was detected by qPCR.The relative length of telomeres was detected by qPCR.The expression of aging proteins P16,P21,P53,and P27 was detected by western blot assay.Cell proliferation was detected by CCK-8 assay.Annexin V-PE/7-AAD apoptosis kit was used to detect the degree of cell apoptosis.RESULTS AND CONCLUSION:Bone marrow-derived mesenchymal stem cell lines overexpressing TCAB1 gene had decreased expression of senescence related genes and proteins,increased Telomere relative length,stronger cell proliferation,less apoptosis,and a youthful state.The expression of age-related genes and proteins in bone marrow mesenchymal stem cells interfering with TCAB1 gene increased,and the relative telomere length decreased;cell proliferation ability was weak;cell apoptosis was more,and cells showed senescence.These results indicate that increasing the expression of TCAB1 in an appropriate range can delay the rate of cell senescence.

Objective:To investigate the relationship between 21-gene recurrence risk score (21-Gene RS) and the prognosis and clinicopathological features of hormone receptor (HR) positive, HER2-negative early breast cancer patients who did not receive neoadjuvant therapy.Methods:A total of 469 patients with HR positive and HER2-negative early breast cancer who received surgical treatment in the First Affiliated Hospital, Zhejiang University School of Medicine from January 2014 to October 2017 were selected. Their clinicopathological data were retrospectively analyzed. Tumor tissue samples were collected from patients, and the expression of 21-gene was detected by reverse transcription quantitative real-time polymerase chain reaction (RT-qPCR). The 21-Gene RS was calculated according to the Trial Assigning Individualized Options for Treatment (TAILORx) RS grouping and National Surgical Adjuvant Breast and Bowel Project B-20 (NSABP B-20) RS grouping principles. Patients were divided into low (21-Gene RS<11 or 21-Gene RS<18), intermediate (11≤21-Gene RS<26 or 18≤21-Gene RS<31) and high (21-Gene RS≥26 or 21-Gene RS≥31) risk groups, and the clinicopathological features and prognostic differences of patients in different risk groups were compared. Statistical data were compared by chi-square test. Survival analysis was performed using Kaplan-Meier curve analysis and the differences between groups were compared using Log-rank test. Multivariate analysis was conducted by COX regression analysis.Results:Based on TAILORx RS grouping, the proportions of low-risk, intermediate-risk and high-risk groups among the 469 patients were 18.8% (88/469), 48.2% (226/469) and 33.0% (155/469), respectively. Based on NSABP B-20 RS grouping, the proportion of low-risk, intermediate-risk and high-risk groups were 43.1% (202/469), 37.5% (176/469) and 19.4% (91/469), respectively. The association of 21-Gene RS with histological grading, luminal typing, Ki-67 expression, and chemotherapy and treatment modalities were statistically significant ( P<0.05) regardless of TAILORx RS grouping or NSABP B-20 RS grouping. Kaplan-Meier survival curve suggested poor prognosis in high-risk group ( P<0.05, Log-rank test). Multivariate COX regression analysis showed that surgical method and 21-Gene RS were risk factors affecting the prognosis of patients. Conclusions:21-Gene RS is significantly associated with the prognosis of patients with HR-positive, HER2-negative, early-stage breast cancer not receiving neoadjuvant therapy, as well as with their clinicopathological characteristics such as patients′ histologic grade, luminal typing, Ki-67 expression, and whether or not they are treated with chemotherapy or other treatment modalities.The 21-Gene RS threshold of 11 and 26 or 18 and 31 can be used to grade the prognosis in Chinese patients with early-stage breast cancer. More researches are needed to guide the selection of postoperative adjuvant therapy for patients with HR-positive and HER2-negative early-stage breast cancer.

Spinal cord injury and regeneration involves transcriptional activity of many genes, of which many remain unknown. Using the rat spinal cord full- transection model, bioinformatics, cloning, expression assays, fusion proteins, and transfection techniques, we identified and characterized one such differentially expressed gene, termed scirr1 (spinal cord injury and/or regeneration related gene 1). Fourteen orthologs were found in 13 species from echinoderm to insect and human by Blast search of NCBI protein reference sequence database. However, no further information is available for these homologues. Using whole-mount in situ hybridization, mouse scirr1 mRNA was expressed temporally and spatially in accordance with the early development sequence of the central nervous system. In adult rat spinal cord, expression of scirr1 mRNA was localized to neurons of gray matter by in situ hybridization. Using immunohistochemistry, SCIRR1 protein was found to be up-regulated and expressed more highly in spinal cord neurons farther from the epicenter of injury. Although the precise function of SCIRR1 is unknown, its unique pattern of expression during CNS early development and up-regulation after spinal cord injury suggest that SCIRR1 should be involved in the succeeding injury and/or repair processes of the injured spinal cord. Also, the typical F-box and leucine-rich repeat (LRR) architecture of rat SCIRR1 indicated that it may play an important substrate recruiting role in the pleiotropic ubiquitin/proteasome pathway. All these make scirr1 a new interesting start to study the spinal cord injury and regeneration mechanism.
Amino Acid Sequence ; Animals ; Base Sequence ; Brain/embryology/metabolism ; Embryo, Mammalian/metabolism ; F-Box Proteins/*biosynthesis ; Gene Expression Regulation, Developmental ; Male ; Mice ; Molecular Sequence Data ; Organ Specificity ; PC12 Cells ; Phylogeny ; Rats ; Rats, Wistar ; Spinal Cord/embryology/metabolism ; Spinal Cord Injuries/*metabolism ; Up-Regulation