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Jin’e Wan,Jian Yang,Cuixia Qiao,Xiaomei Sun,Aiting Di,Lize Zhang,Dandan Wang,Gang Zhao 연세대학교의과대학 2019 Yonsei medical journal Vol.60 No.5
Purpose: Colorectal cancer (CRC) is the third most common cancer in China and poses high morbidity and mortality. In recentyears, increasing evidence has indicated that microRNAs played important functions in the occurrence and development of tumors. The purpose of this study was to identify the biological mechanisms of miR-362 in CRC. Materials and Methods: Quantitative real-time PCR was carried out to assess the expression of miR-362 and SIX1. The Kaplan-Meier method was employed to evaluate the 5-year overall survival of CRC patients. The proliferative and invasive abilities of CRCcells were assessed by MTT and transwell assays. Results: miR-362 was significantly decreased in CRC tissues and cell lines, compared to the normal tissues and normal cells. Asignificant connection was confirmed between the overall survival of 53 CRC patients and low expression of miR-362. Downregulationof miR-362 inhibited the proliferation and invasion through binding to the 3'-UTR of SIX1 mRNA in CRC. Additionally, wediscovered that SIX1 was a direct target gene of miR-362 and that the expression of miR-362 had a negative connection with SIX1expression in CRC. SIX1 could reverse partial functions in the proliferation and invasion in CRC cells. Conclusion: miR-362 may be a prognostic marker in CRC and suppress CRC cell proliferation and invasion in part through targetingthe 3'-UTR of SIX1 mRNA. The newly identified miR-362/SIX1 axis provides insight into the progression of CRC.
( Hai Yan Zhao ),( Hui Ying Li ),( Jian Jin ),( Ji Zhe Jin ),( Long Ye Zhang ),( Mei Ying Xuan ),( Xue Mei Jin ),( Yu Ji Jiang ),( Hai Lan Zheng ),( Ying Shun Jin ),( Yong Jie Jin ),( Bum Soon Choi ) 대한내과학회 2021 The Korean Journal of Internal Medicine Vol.36 No.0
Background/Aims: Accumulating evidence indicates that L-carnitine (LC) protects against multiorgan damage through its antioxidant properties and preservation of the mitochondria. Little information is available about the effects of LC on renal fibrosis. This study examined whether LC treatment would provide renoprotection in a rat model of unilateral ureteral obstruction (UUO) and in vitro. Methods: Sprague-Dawley rats that underwent UUO were treated daily with LC for 7 or 14 days. The influence of LC on renal injury caused by UUO was evaluated by histopathology, and analysis of gene expression, oxidative stress, mitochondrial function, programmed cell death, and phosphatidylinositol 3-kinase (PI3K)/ AKT/forkhead box protein O 1a (FoxO1a) signaling. In addition, H<sub>2</sub>O<sub>2</sub>-exposed human kidney cells (HK-2) were treated with LC. Results: LC treatment inhibited expression of proinflammatory and profibrotic cytokines, and was followed by a significant attenuation of tubulointerstitial inflammation and fibrosis. The increased oxidative stress caused by UUO was associated with mitochondrial dysfunction and excessive apoptosis and autophagy via PI3K/AKT/FoxO1a-dependent signaling, and this was abrogated by administration of LC. In H<sub>2</sub>O<sub>2</sub>-exposed HK-2 cells, LC decreased intracellular production of reactive oxygen species, and suppressed expression of profibrotic cytokines and reduced the number of apoptotic cells. Conclusions: LC protects against the progression of tubulointerstitial fibrosis in an obstructed kidney.
( Jian Jin ),( Sun Woo Lim ),( Long Jin ),( Ji Hyun Yu ),( Hyun Seon Kim ),( Byung Ha Chung ),( Chul Woo Yang ) 대한내과학회 2017 The Korean Journal of Internal Medicine Vol.32 No.2
Background/Aims: Metformin (MET) is a first-line drug for type 2 diabetes mellitus (DM); its effect on new-onset diabetes after transplantation caused by immunosuppressant therapy is unclear. We compared the effects of MET on DM caused by tacrolimus (TAC) or sirolimus (SRL). Methods: DM was induced by injection of TAC (1.5 mg/kg) or SRL (0.3 mg/kg) for 2 weeks in rats, and MET (200 mg/kg) was injected for 2 more weeks. The effects of MET on DM caused by TAC or SRL were evaluated using an intraperitoneal glucose tolerance test (IPGTT) and by measuring plasma insulin concentration, islet size, and glucose-stimulated insulin secretion (GSIS). The effects of MET on the expression of adenosine monophosphate-activated protein kinase (AMPK), a pharmacological target of MET, were compared between TAC- and SRL-treated islets. Results: IPGTT showed that both TAC and SRL induced hyperglycemia and reduced plasma insulin concentration compared with vehicle. These changes were reversed by addition of MET to SRL but not to TAC. Pancreatic islet cell size was decreased by TAC but not by SRL, but addition of MET did not affect pancreatic islet cell size in either group. MET significantly increased GSIS in SRL- but not in TAC-treated rats. AMPK expression was not affected by TAC but was significantly decreased in SRL-treated islets. Addition of MET restored AMPK expression in SRL-treated islets but not in TAC-treated islets. Conclusions: MET has different effects on hyperglycemia caused by TAC and SRL. The discrepancy between these drugs is related to their different mechanisms causing DM.
Jin, Jian-Ming,Lee, Seunghoon,Lee, Jungkwan,Baek, Seung-Ryul,Kim, Jin-Cheol,Yun, Sung-Hwan,Park, Sook-Young,Kang, Seogchan,Lee, Yin-Won Blackwell Publishing Ltd 2010 Molecular microbiology Vol.76 No.2
<P>Summary</P><P>Apicidin is a cyclic tetrapeptide produced by certain isolates of <I>Fusarium semitectum</I> and has been shown to inhibit Apicomplexan histone deacetylase. An apicidin-producing strain (KCTC16676) of the filamentous fungus was mutated using an <I>Agrobacterium tumefaciens</I>-mediated transformation, resulting in 24 apicidin-deficient mutants. Three of the mutants had a T-DNA insertion in a gene that encodes a non-ribosomal peptide synthetase (NRPS). Results of sequence, expression, and gene deletion analyses defined an apicidin biosynthetic gene cluster, and the NRPS gene was named as apicidin synthetase gene 1 (<I>APS1</I>). A 63 kb region surrounding <I>APS1</I> was sequenced and analysis revealed the presence of 19 genes. All of the genes including <I>APS1</I> were individually deleted to determine their roles in apicidin biosynthesis. Chemical analyses of the mutant strains showed that eight genes are required for apicidin production and were used to propose an apicidin biosynthetic pathway. The apicidin analogues apicidin E, apicidin D<SUB>2</SUB> and apicidin B were identified from chemical analysis of the mutants. The cluster gene <I>APS2</I>, a putative transcription factor, was shown to regulate expression of the genes in the cluster and overexpression of <I>APS2</I> increased apicidin production. This study establishes the apicidin biosynthetic pathway and provides new opportunities to improve the production of apicidin and produce new analogues.</P>
Jin, Jian,Zhou, Wei-Jie,Chen, Ying,Liu, Yi-Long,Sun, Xiao-Qiang,Xi, Hai-Tao Korean Chemical Society 2014 Bulletin of the Korean Chemical Society Vol.35 No.2
Two classes of morpholino-substitued thioacetate have been successfully synthesized and their electrochemical properties of self-assembled monolayers (SAMs) on Au electrode are measured by cyclic voltammetry (CV) and electrochemical impedance spectroscopy (EIS). The barrier property of the SAMs-modified surfaces is evaluated by using potassium ferro/ferri cyanide. The results suggest that the arenethioacetate forms higher-quality close-packed blocking monolayers in comparison with alkanethioacetate. Furthermore, it has shown that the barrier properties of these monolayers can be significantly improved by mixed SAMs formation with decanethiol. From our experimental results we find that the electron transfer reaction of $[Fe(CN)_6]^{3/4-}$ redox couple occurs predominantly through the pinholes and defects present in the SAM and both SAMs show a good and fast capacity in recognition for $Ag^+$. The morphological and elementary composition have also been examined by scanning electron microscope (SEM) and energy dispersive spectrometer (EDS).