Objective SUMO-specific protease 3(SENP3),a member of the SUMO-specific protease family,reverses the SUMOylation of SUMO-2/3 conjugates.Dysregulation of SENP3 has been proven to be involved in the development of vario...Objective SUMO-specific protease 3(SENP3),a member of the SUMO-specific protease family,reverses the SUMOylation of SUMO-2/3 conjugates.Dysregulation of SENP3 has been proven to be involved in the development of various tumors.However,its role in mantle cell lymphoma(MCL),a highly aggressive lymphoma,remains unclear.This study was aimed to elucidate the effect of SENP3 in MCL.Methods The expression of SENP3 in MCL cells and tissue samples was detected by RT-qPCR,Western blotting or immunohistochemistry.MCL cells with stable SENP3 knockdown were constructed using short hairpin RNAs.Cell proliferation was assessed by CCK-8 assay,and cell apoptosis was determined by flow cytometry.mRNA sequencing(mRNA-seq)was used to investigate the underlying mechanism of SENP3 knockdown on MCL development.A xenograft nude mouse model was established to evaluate the effect of SENP3 on MCL growth in vivo.Results SENP3 was upregulated in MCL patient samples and cells.Knockdown of SENP3 in MCL cells inhibited cell proliferation and promoted cell apoptosis.Meanwhile,the canonical Wnt signaling pathway and the expression of Wnt10a were suppressed after SENP3 knockdown.Furthermore,the growth of MCL cells in vivo was significantly inhibited after SENP3 knockdown in a xenograft nude mouse model.Conclusion SENP3 participants in the development of MCL and may serve as a therapeutic target for MCL.展开更多
Perpendicular synthetic-antiferromagnet(p-SAF) has broad applications in spin-transfer-torque magnetic random access memory and magnetic sensors. In this study, the p-SAF films consisting of (Co/Ni)3]/Ir(tIr)/[(Ni/Co)...Perpendicular synthetic-antiferromagnet(p-SAF) has broad applications in spin-transfer-torque magnetic random access memory and magnetic sensors. In this study, the p-SAF films consisting of (Co/Ni)3]/Ir(tIr)/[(Ni/Co)3are fabricated by magnetron sputtering technology. We study the domain structure and switching field distribution in p-SAF by changing the thickness of the infrared space layer. The strongest exchange coupling field(Hex) is observed when the thickness of Ir layer(tIr) is 0.7 nm and becoming weak according to the Ruderman–Kittel–Kasuya–Yosida-type coupling at 1.05 nm,2.1 nm, 4.55 nm, and 4.9 nm in sequence. Furthermore, the domain switching process between the upper Co/Ni stack and the bottom Co/Ni stack is different because of the antiferromagnet coupling. Compared with ferromagnet coupling films, the antiferromagnet samples possess three irreversible reversal regions in the first-order reversal curve distribution.With tIrincreasing, these irreversible reversal regions become denser and smaller. The results from this study will help us understand the details of the magnetization reversal process in the p-SAF.展开更多
基金supported by the Chongqing Natural Science Foundation(No.2023NSCQ-MSX3161 and No.cstc2020jcyj-msxmX1058)the National Natural Science Foundation of China(No.81800172).
文摘Objective SUMO-specific protease 3(SENP3),a member of the SUMO-specific protease family,reverses the SUMOylation of SUMO-2/3 conjugates.Dysregulation of SENP3 has been proven to be involved in the development of various tumors.However,its role in mantle cell lymphoma(MCL),a highly aggressive lymphoma,remains unclear.This study was aimed to elucidate the effect of SENP3 in MCL.Methods The expression of SENP3 in MCL cells and tissue samples was detected by RT-qPCR,Western blotting or immunohistochemistry.MCL cells with stable SENP3 knockdown were constructed using short hairpin RNAs.Cell proliferation was assessed by CCK-8 assay,and cell apoptosis was determined by flow cytometry.mRNA sequencing(mRNA-seq)was used to investigate the underlying mechanism of SENP3 knockdown on MCL development.A xenograft nude mouse model was established to evaluate the effect of SENP3 on MCL growth in vivo.Results SENP3 was upregulated in MCL patient samples and cells.Knockdown of SENP3 in MCL cells inhibited cell proliferation and promoted cell apoptosis.Meanwhile,the canonical Wnt signaling pathway and the expression of Wnt10a were suppressed after SENP3 knockdown.Furthermore,the growth of MCL cells in vivo was significantly inhibited after SENP3 knockdown in a xenograft nude mouse model.Conclusion SENP3 participants in the development of MCL and may serve as a therapeutic target for MCL.
基金Project supported by the Natural Science Foundation of Gansu Province, China (Grant No. 22JR5RA775)the Science and Technology Program of Lanzhou, China (Grant No. 2021-1-157)+2 种基金the Guangdong Basic and Applied Basic Research Foundation, China (Grant Nos. 2020A1515110998 and 2022A1515012123)the Outstanding Youth Foundation of Gansu Academy of Science, China (Grant No. 2021YQ01)the Innovative Team Construction Project of Gansu Academy of Sciences, China (Grant No. 2020CX005-01)。
文摘Perpendicular synthetic-antiferromagnet(p-SAF) has broad applications in spin-transfer-torque magnetic random access memory and magnetic sensors. In this study, the p-SAF films consisting of (Co/Ni)3]/Ir(tIr)/[(Ni/Co)3are fabricated by magnetron sputtering technology. We study the domain structure and switching field distribution in p-SAF by changing the thickness of the infrared space layer. The strongest exchange coupling field(Hex) is observed when the thickness of Ir layer(tIr) is 0.7 nm and becoming weak according to the Ruderman–Kittel–Kasuya–Yosida-type coupling at 1.05 nm,2.1 nm, 4.55 nm, and 4.9 nm in sequence. Furthermore, the domain switching process between the upper Co/Ni stack and the bottom Co/Ni stack is different because of the antiferromagnet coupling. Compared with ferromagnet coupling films, the antiferromagnet samples possess three irreversible reversal regions in the first-order reversal curve distribution.With tIrincreasing, these irreversible reversal regions become denser and smaller. The results from this study will help us understand the details of the magnetization reversal process in the p-SAF.