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| 1 | Integrated transcriptomic and metabolomic analyses of a wax deficient citrus mutant exhibiting jasmonic acid-mediated defense against fungal pathogens显示文摘Naturally,resistant crop germplasms are important resources for managing the issues of agricultural product safety and environment deterioration.We found a spontaneous mutant of‘Newhall’navel orange(Citrus sinensis Osbeck)(MT)with broad-spectrum protections against fungal pathogens in the orchard,postharvest-storage,and artificial inoculation conditions.To understand the defense mechanism of MT fruit,we constructed a genome-scale metabolic network that integrated metabolome and transcriptome datasets.The coordinated transcriptomic and metabolic data were enriched in two sub-networks,showing the decrease in very long chain fatty acid(by 41.53%)and cuticular wax synthesis(by 81.34%),and increase in the synthesis of jasmonic acid(JA)(by 95.23%)and JA-induced metabolites such as 5-dimethylnobietin(by 28.37%)in MT.Furthermore,cytological and biochemical analyses confirmed that the response to fungal infection in MT was independent of wax deficiency and was correlated with the levels of jasmonates,and the expression of plant defensin gene PDF1.2.Results of exogenous application of MeJA and JA inhibitors such as propyl gallate proved that JA-mediated defense contributes to the strong tolerance against pathogens in MT.Our results indicated that jasmonate biosynthesis and signaling are stimulated by the fatty acid redirection of MT,and participate in the tolerance of pathogenic fungi. | Yizhong He Jingwen Han Runsheng Liu Yuduan Ding Jinqiu Wang Li Sun Xiaoming Yang Yunliu Zeng Weiwei Wen Juan Xu Hongming Zhang Xiang Yan Zhaoxing Chen Zuliang Gu Hong Chen Huanqing Tang Xiuxin Deng Yunjiang Cheng | 2018 | Horticulture Research2018，5，1： | 8 |
| 2 | Absence of FHIT expression is associated with apoptosis inhibition in colorectal cancer显示文摘Objective: To investigate the expression of fragile histidine triad (FHIT) protein in normal colorectal tissue, colorectal adenoma and colorectal cancer (CRC), and to study the relationships between the expression of FHIT protein and the clinical pathology, the apoptosis-associated protein (Bcl-2, Bax, Survivin), apoptosis in colorectal cancer. Methods: Tissue microarray (TMA) and immunohistochemistry SP were used to detect the expression of FHIT gene, Bcl-2, Bax and Survivin in 16 cases of the normal colorectal tissue, 16 cases of colorectal adenoma and 80 cases of the colorectal cancer. TUNEL was used to detect the apoptosis index (AI) in 80 cases of the colorectal cancer. Results: (1) The positive rates of FHIT gene expression in normal colorectal tissue, colorectal adenoma and adenocancer were 93.75%, 68.75% and 46.25% respectively. There were no significant differences in the relationships between the FHIT gene expression and histological types, the gender as well as the age (P>0.05). There were significant relationships between FHIT gene expression and lymph node metastasis, histological grades, Duke’s system as well as the 5-year survival rate after operation. (2) The positive rates of Bax, Bcl-2 and Survivin in colorectal adenocancer were 72.50%, 51.25%, 77.50% respectively. The expression of FHIT gene was positively correlated with that of Bcl-2, Bax and Survivin. (3) The mean AI in FHIT negative tumors was significantly lower than that in FHIT positive tumors (P<0.01). Conclusion: FHIT gene may play a role in the oncogenesis and progression of colorectal cancer. The abnormal regulation of apoptosis may play an important role in the pathogenesis of colorectal cancer. | Jie Cao Xiaoping Chen Wanglin Li Jie Xia Hong Du Weibiao Tang Hui Wang Xiwen Chen Huanqing Xiao Yuyuan Li | 2007 | The Chinese-German Journal of Clinical Oncology2007，6，1： | 1 |
| 3 | Targeting Kindlin-2 in adipocytes increases bone mass through inhibiting FAS/PPARγ/FABP4 signaling in mice显示文摘Osteoporosis(OP)is a systemic skeletal disease that primarily affects the elderly population,which greatly increases the risk of fractures.Here we report that Kindlin-2 expression in adipose tissue increases during aging and high-fat diet fed and is accompanied by decreased bone mass.Kindlin-2 specific deletion(K2KO)controlled by Adipoq-Cre mice or adipose tissue-targeting AAV(AAV-Rec2-CasRx-sgK2)significantly increases bone mass.Mechanistically,Kindlin-2 promotes peroxisome proliferator-activated receptor gamma(PPARγ)activation and downstream fatty acid binding protein 4(FABP4)expression through stabilizing fatty acid synthase(FAS),and increased FABP4 inhibits insulin expression and decreases bone mass.Kindlin-2 inhibition results in accelerated FAS degradation,decreased PPARγactivation and FABP4 expression,and therefore increased insulin expression and bone mass.Interestingly,we find that FABP4 is increased while insulin is decreased in serum of OP patients.Increased FABP4 expression through PPARγactivation by rosiglitazone reverses the high bone mass phenotype of K2KO mice.Inhibition of FAS by C75 phenocopies the high bone mass phenotype of K2KO mice.Collectively,our study establishes a novel Kindlin-2/FAS/PPARγ/FABP4/insulin axis in adipose tissue modulating bone mass and strongly indicates that FAS and Kindlin-2 are new potential targets and C75 or AAV-Rec2-CasRx-sgK2 treatment are potential strategies for OP treatment. | Wanze Tang Zhen Ding Huanqing Gao Qinnan Yan Jingping Liu Yingying Han Xiaoting Hou Zhengwei Liu Litong Chen Dazhi Yang Guixing Ma Huiling Cao | 2023 | Acta Pharmaceutica Sinica B2023，13，11： | 0 |
| 4 | Absence of FHIT expression is associated with apoptosis inhibition in colorectal cancer显示文摘The fragile histidine triad(FHIT)gene,a candidate tumor suppressor gene located at 3p14.2,has been shown to be involved in the carcinogenesis of many human tissues,including digestive tract tissues.However,the expression and the role of the FHIT in the initiation and the development of the colorectal cancer(CRC)are poorly understood.We have shown that the FHIT gene exhibits significantly decreased expression in human CRC compared to colorectal adenoma and normal colorectal tissue by tissue microarray(TMA).The positive rate of FHIT gene expression in normal colorectal tissue,adenoma and adenocarcinoma were 93.75%,68.75%and 46.25%,respectively.We show this decreased expression to be significantly correlated with the progression of colorectal carcinoma(P<0.05)as well as with differentiation and lymph node metastasis(P<0.05).We detected two somatic alterations in the FHIT gene in human CRC.The presence of this mutation correlated significantly with decreased FHIT expression in the human CRC.In our present study we tested the hypothesis that the decreased FHIT expression resulted in apoptosis inhibition associated with abnormal expression of apoptosis related proteins.To test this hypothesis we did a series of experiments.In the first test,we assessed apoptosis status using a standard TUNEL(terminal deoxynucleotidyl transferase-mediated dUTP nick-end-labeling)assay by comparing FHIT-positive CRC vs.FHIT-negative CRC.In the second experiment,the protein expression of the FHIT and other apoptosis related proteins(Bax,Bcl-2 and Survivin)were measured in human CRC by TMA.Our combined results demonstrate the mutation in the FHIT gene significantly reduced FHIT expression in human CRC.Both TUNEL and TMA experiments demonstrated significantly inhibited apoptosis by down-regulation of Bax and the up-regulation of Survivin and Bcl-2.Collectively,these studies identify the mechanism by which an important tumor suppressor gene,FHIT is inactivated specifically in human CRC contributing to our understanding of the mechanism of colorectal carcinogenesis. | CAO Jie CHEN Xiaoping LI Wanglin XIA Jie DU Hong TANG Weibiao CHEN Shanming WANG Hui CHEN Xiwen XIAO Huanqing LI Yuyuan | 2007 | Frontiers of Medicine2007，1，2： | 0 |
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