作者机构：
Department of Neurosurgery, Chenzhou No.1 People's Hospital, Hunan, Chenzhou, 423000, China;Electrocardiographic room, Chenzhou No.1 People's Hospital, Hunan, Chenzhou, 423000, China;Department of Pathophysiology, University of South China, Hunan, Hengyang, 421001, China
摘要：
<jats:sec><jats:title>Background</jats:title><jats:p>The extent of bowel resection is widely debated in colon cancer surgery. Right hemicolectomy (RHC) and partial colectomy (PC) are the most common operation options for right-sided colon cancer (RCC). However, there are still no treatment guidelines or published studies to guide surgical options for mucinous adenocarcinoma (MAC) of RCC.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>Patients with MAC and non-specific adenocarcinoma (AC) of RCC who underwent RHC and PC from 2010 to 2015 in the Surveillance, Epidemiology, and End Results (SEER) database were retrieved. The general characteristics and survival were compared and analyzed.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>A total of 27,910 RCC patients were enrolled in this study, among them 3,413 were MAC. The results showed that race, carcinoembryonic antigen (CEA) level, perineural invasion (PNI), tumor size, tumor location, TNM stage, liver metastasis, chemotherapy were significantly different between MAC and AC groups. The MAC group had similar dissected lymph nodes, but more positive lymph nodes than the AC group. The overall survival (OS) of the MAC group was poorer than that of the AC group, but cancer-specific survival (CSS) was similar between the two groups. The RHC subgroup of the MAC group had more patients of age ≤60 years, larger tumor size, cecum/ascending colon location and dissected lymph nodes than the PC subgroup, but similar positive lymph nodes, perioperative mortality, OS and CSS as the PC subgroup. Moreover, the univariate and multivariable analyses for the survival of RCC patients with MAC showed that RHC might not be a superior predictor for OS and CSS compared with PC.</jats:p></jats:sec><jats:sec><jats:title>Conclusions</jats:title><jats:p>RHC could not dissect more positive lymph nodes or provide long-term survival benefits for RCC patients with MAC compared with PC. This study could provide some evidence for surgery treatment selection for MAC of RCC, which has important clinical value in individual management of colon cancer patients.</jats:p></jats:sec>
摘要：
<jats:title>Abstract</jats:title><jats:sec>
<jats:title>Background</jats:title>
<jats:p>Mucinous adenocarcinoma (MC) is the second most common pathological type of colon carcinoma (CC). Colon cancer liver metastases (CLMs) are common and lethal, and complete resection of the primary tumour and metastases for CLM patients would be beneficial. However, there is still no consensus on the role of surgery for MC with liver metastases (M-CLM).</jats:p>
</jats:sec><jats:sec>
<jats:title>Methods</jats:title>
<jats:p>Patients diagnosed with M-CLM or classical adenocarcinoma with CLM (A-CLM) from 2010 to 2013 in the Surveillance, Epidemiology, and End Results (SEER) database were retrieved. The clinicopathological features and overall survival (OS) and cancer-specific survival (CSS) data were compared and analysed.</jats:p>
</jats:sec><jats:sec>
<jats:title>Results</jats:title>
<jats:p>The results showed that the M-CLM group had a larger tumour size, more right colon localizations, higher pT and pN stages, more female patients, and more retrieved and positive lymph nodes and accounted for a higher proportion of surgeries than the A-CLM group. The OS and CSS of M-CLM patients who underwent any type of surgery were significantly better than those of patients who did not undergo any surgery, but poorer than those of A-CLM patients who underwent surgery. Meanwhile, the OS and CSS of M-CLM and A-CLM patients who did not undergo any surgery were comparable. Compared with hemicolectomy, partial colectomy led to similar or better OS and CSS for M-CLM, and surgery was an independent protective factor for long-term survival in M-CLM.</jats:p>
</jats:sec><jats:sec>
<jats:title>Conclusions</jats:title>
<jats:p>M-CLM had distinct clinicopathological characteristics from A-CLM, and surgery could improve the survival and is an independent favourable prognostic factor for M-CLM. In addition, partial colectomy might be a non-inferiority choice as hemicolectomy for M-CLM according to the results from this study.</jats:p>
</jats:sec>
期刊：
CELL DEATH & DISEASE,2020年11(10):908 ISSN：2041-4889
通讯作者：
Li, Xiaorong;Lin, Changwei
作者机构：
[Li, Xiaorong; Yu, Bowen; Wu, Hao; Wu, Runliu; Bai, Yang; Xie, Canbin; Zhang, Yi; Lin, Changwei] Cent South Univ, XiangYa Hosp 3, Dept Gastrointestinal Surg, Changsha 410013, Hunan, Peoples R China.;[Li, Liang] Univ South China, Sch Med, Five Year Program Clin Med, Hengyang 421001, Hunan, Peoples R China.;[Huang, Lihua] Cent South Univ, XiangYa Hosp 3, Ctr Expt Med, Changsha 410013, Hunan, Peoples R China.;[Yan, Yichao] Peking Univ Int Hosp, Dept Gastroenterol Surg, Beijing 102206, Peoples R China.;[Lin, Changwei] Cent South Univ, Sch Life Sci, Changsha 410078, Hunan, Peoples R China.
通讯机构：
[Xiaorong Li; Changwei Lin] D;Department of Gastrointestinal surgery, The Third XiangYa Hospital of Central South University, Changsha, Hunan, 410013, China.;School of Life Sciences, Central South University, Changsha, Hunan, 410078, China.
摘要：
The long noncoding RNA (lncRNA) LUCAT1 was recently reported to be upregulated and to play an essential role in multiple cancer types, especially colorectal cancer (CRC), but the molecular mechanisms of LUCAT1 in CRC are mostly unreported. Here, a systematic analysis of LUACT1 expression is performed with data from TCGA database and clinic CRC samples. LUCAT1 is identified as a putative oncogene, which is significantly upregulated in CRC and is associated with poor prognosis. Loss of LUCAT1 restricts CRC proliferative capacities in vitro and in vivo. Mechanically, NCL is identified as the protein binding partner of LUCAT1 by using chromatin isolation by RNA purification coupled with mass spectrometry (ChIRP-MS) and RNA immunoprecipitation assays. We also show that NCL directly binds to LUCAT1 via its putative G-quadruplex-forming regions from nucleotides 717 to 746. The interaction between LUCAT1 and NCL interferes NCL-mediated inhibition of MYC and promote the expression of MYC. Cells lacking LUCAT1 show a decreased MYC expression, and NCL knockdown rescue LUCAT1 depletion-induced inhibition of CRC cell proliferation and MYC expression. Our results suggest that LUCAT1 plays a critical role in CRC cell proliferation by inhibiting the function of NCL via its G-quadruplex structure and may serve as a new prognostic biomarker and effective therapeutic target for CRC.
作者机构：
[Tang, Yan-Ni; Gao, Yuan-Yuan; Xiang, Ju; Gao, YY; Li, Jian-Ming] Changsha Med Univ, Neurosci Res Ctr, Sch Basic Med Sci, Changsha 410219, Peoples R China.;[Wang, Zhi-Zhong; Xiang, Ju] Hunan First Normal Univ, South City Coll, Changsha 410205, Peoples R China.;[Xiang, Ju; Zhang, Yan] Cent S Univ, Sch Comp Sci & Engn, Changsha 410083, Peoples R China.;[Li, Hui-Jia] Beijing Univ Posts & Telecommun, Sch Sci, Beijing 100876, Peoples R China.;[Zhang, Yan; Chen, Shi] Changsha Med Univ, Dept Informat Sci & Engn, Changsha 410219, Peoples R China.
通讯机构：
[Xiang, J; Gao, YY; Xiang, Ju] C;[Xiang, Ju] H;[Li, Hui-Jia] B;Changsha Med Univ, Neurosci Res Ctr, Sch Basic Med Sci, Changsha 410219, Peoples R China.;Hunan First Normal Univ, South City Coll, Changsha 410205, Peoples R China.
关键词：
Community detection;Complex networks;Disease gene;Disease module;Surprise
摘要：
Although the Epstein-Barr virus (EBV) is a well-known human oncogenic virus, its molecular mechanisms involved in the transformation of healthy human cells remain poorly understood. In this study, human lymphocytes were isolated from the peripheral blood of healthy adults, and lymphocytes were transformed in vitro by EBV. Agilent human whole genome microarrays were used to detect the differential gene expression profiles of EBV-transformed lymphoblasts and healthy peripheral blood lymphocytes (PBLs). By constructing the gene functional network of EBV-induced lymphocyte transformation, we screened out candidate key genes in this process and verified their expression levels by real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot. In the EBV-transformed lymphoblasts, 2335 differentially expressed genes, including 1328 up-regulated and 1007 down-regulated, were screened out. Five candidate key genes, namely, PLK1, E2F1, PTPN11, BIRC5 and FYN were mainly screened out according to the results of LIMMA, String, Cytoscape software analysis. RT-qPCR and Western blot showed that PLK1, E2F1, PTPN11, BIRC5 genes had increased expression levels, and FYN gene was down-regulated in EBV-transformed lymphoblasts. Silencing of PLK1 gene in Raji cells could inhibit cell proliferation and invasion, and induce cell cycle arrest and apoptosis. In conclusion, PLK1, E2F1, PTPN11, BIRC5 and FYN are the candidate key molecules of EBV-transformed lymphocytes.
摘要：
BACKGROUND: Salinomycin is a monocarboxylic polyether antibiotic and is a potential chemotherapy drug. Our previous studies showed that salinomycin inhibited cell growth and targeted CSCs in prostate cancer. However, the precise target of salinomycin action is unclear. METHODS: In this work, we analyzed and identified differentially expressed genes (DEGs) after treatment with or without salinomycin using a gene expression microarray in vitro (PC-3 cells) and in vivo (NOD/SCID mice xenograft model generated from implanted PC-3 cells). Western blotting and immunohistochemical staining were used to analyze the expression of ATP2A3 and endoplasmic reticulum (ER) stress biomarkers. Flow cytometry was used to analyze the cell cycle, apoptosis and intracellular Ca(2+) concentration. RESULTS: A significantly upregulated gene, ATPase sarcoplasmatic/endoplasmatic reticulum Ca(2+) transporting 3 (ATP2A3), was successfully identified. In subsequent studies, we found that ATP2A3 overexpression could trigger ER stress and exert anti-cancer effects in PC-3 and DU145 cells. ATP2A3 was slightly expressed, but the ER stress biomarkers showed strong staining in prostate cancer tissues. We also found that salinomycin could trigger ER stress, which might be related to ATP2A3-mediated Ca(2+) release in PC-3 cells. Furthermore, we found that salinomycin-triggered ER stress could promote apoptosis and thus exert anti-cancer effects in prostate cancer cells. CONCLUSION: This study demonstrates that ATP2A3 might be one of the potential targets for salinomycin, which can inhibit Ca(2+) release and trigger ER stress to exert anti-cancer effects.
作者机构：
[Yao Yao; Zhong J.; Yang X.; Wang J.] Institute of Clinical Medicine, First Affiliated Hospital of University of South China, Hengyang, 421001, China;Department of Metabolism and Endocrinology, Second Affiliated Hospital of University of South China, Hengyang, 421001, China;[Dai X.] Department of General Surgery, Second Affiliated Hospital of University of South China, Hengyang, 421001, China;[Zhang Y.] Institute of Clinical Medicine, Second Affiliated Hospital of University of South China, Hengyang, 421001, China;Department of Metabolism and Endocrinology, First Affiliated Hospital of University of South China, Hengyang, 421001, China
通讯机构：
[Gebo Wen; Jing Zhong] I;Institute of Clinical Medicine, The First Affiliated Hospital of University of South China, Hengyang, China<&wdkj&>Institute of Clinical Medicine, The First Affiliated Hospital of University of South China, Hengyang, China<&wdkj&>Department of Metabolism and Endocrinology, The First Affiliated Hospital of University of South China, Hengyang, China
摘要：
Autophagy as a novel therapeutic target can inhibit or increase treatment efficacy in various types of breast cancer in a cell-type-dependent manner [1,2].Several studies have revealed that the coordination between Akt and the glycolytic pathway plays an indispensable role in mediating autophagy and caspase-dependent apoptosis,suggesting that a new regulatory mechanism for the process [3,4].Protein arginine N-methyltransferases(PRMTs)are eukaryotic enzymes that catalyze the transfer of methyl groups from S-adenosylmethionine to arginine residues of numerous PRMT substrates [5,6].PRMT2(also known as HRMT1L1)belongs to the arginine methyltransferase family [7].PRMT2β is a novel PRMT2 splice variant isolated from breast cancer cell [8].It occurs at the 3′ end of the PRMT2,resulting in loss of exons 7–9 and downstream frame-shifting [9].PRMT2β possesses 83 new amino acids at the C-terminus and its size is 301 amino acids.Our previous study reported that PRMT2β has potential antitumor effect by suppressing cyclin D1 expression [10].However,little is known about whether PRMT2β could regulate autophagy and glycolysis of MCF-7 cells.
作者机构：
[Jia, Zeming; Chen, Jie; Ding, Chengming; Zhang, Yaoting; Peng, Jian] Cent S Univ, Xiangya Hosp, Dept Gen Surg, Changsha, Hunan, Peoples R China.;[He, Jun; Li, Chong; Ding, Chengming; Zhu, Zhu; Han, Dong] Univ South China, Dept Hepatopancreatobiliary Surg, Affiliated Hosp 1, Hengyang, Peoples R China.;[Li, Junhua; Ding, Chengming; Zhao, Jun] Univ Southern Calif, Dept Mol Microbiol & Immunol, Norris Comprehens Canc Ctr, Los Angeles, CA USA.;[Liao, Wenyan] Univ South China, Dept Obstet & Gynecol, Affiliated Hosp 1, Hengyang, Peoples R China.;[Zeng, Yi] Youjiang Med Univ Nationalities, Dept Pathol & Immunol, Baise, Peoples R China.
通讯机构：
[Peng, Jian; Xia, Zanxian] C;Cent S Univ, Xiangya Hosp, Dept Gen Surg, Changsha, Hunan, Peoples R China.;Cent S Univ, State Key Lab Med Genet, Changsha, Hunan, Peoples R China.;Cent S Univ, Sch Life Sci, Changsha, Hunan, Peoples R China.
摘要：
<jats:title>Abstract</jats:title><jats:sec><jats:title>Objective</jats:title><jats:p>β‐catenin is one of the most critical oncogenes associated with many kinds of human cancers, especially in the human CRC. Innate immunity recognizes tumour derived damage‐associated molecular patterns (DAMPs) and primes the anti‐tumour adaptive responses. While the function of β‐catenin in CRC tumourigenesis is well established, its impact on innate immune evasion is largely unknown. The aim of this study is to characterize the role of β‐catenin in inhibiting RIG‐I‐like receptor (RLR)‐mediated IFN‐β signalling in colorectal cancer.</jats:p></jats:sec><jats:sec><jats:title>Materials and Methods</jats:title><jats:p>Immunohistochemical staining and western blotting were conducted to study the expression of β‐catenin, IRF3 and phospho‐IRF3 (p‐IRF3) in CRC samples and cell lines. Plaque assay determining virus replication was performed to assess the regulation of β‐catenin on IFN‐β signalling. The inhibition of β‐catenin on RLR‐mediated IFN‐β signalling was further studied by real‐time analyses and reporter assays in the context of lentiviral‐mediated β‐catenin stably knocking down. Lastly, co‐immunoprecipitation and nuclear fractionation assay were conducted to monitor the interaction between β‐catenin and IRF3.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>We found that high expression of β‐catenin positively correlated with the expression of IRF3 in CRC cells. Overexpression of β‐catenin increased the viral replication. Conversely knocking down of β‐catenin inhibited viral replication. Furthermore, our data demonstrated that β‐catenin could inhibit the expression of IFN‐β and interferon‐stimulated gene 56 (ISG56). Mechanistically, we found that β‐catenin interacted with IRF3 and blocked its nuclear translocation.</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p>Our study reveals an unprecedented role of β‐catenin in enabling innate immune evasion in CRC.</jats:p></jats:sec>
作者：
Zhang, Yunqiang;Tu, Lijun;Zhou, Xiuhong;Li, Bin
期刊：
Medical science monitor basic research,2018年24:216-224 ISSN：2325-4394
作者机构：
[Li, Bin; Zhang, Yunqiang] Department of Neurosurgery, Chenzhou No. 1 People's Hospital, Chenzhou, Hunan, China (mainland);[Tu, Lijun] Electrocardiographic Room, Chenzhou No. 1 People's Hospital, Chenzhou, Hunan, China (mainland);[Zhou, Xiuhong] Department of Pathophysiology, University of South China, Hengyang, Hunan, China (mainland)
摘要：
BACKGROUND Curcumin has clear anti-tumor activity in various carcinomas. It regulates various signaling pathways like Wnt/β-catenin and JAK2/STAT3, which play vital roles in cell proliferation of several carcinomas, but to the best of our knowledge, there are currently no published reports on human glioma CHME cells. Therefore, the aim of this study was to explore the effect of curcumin on human glioma CHME cells. MATERIAL AND METHODS The CHME cell line was purchased from American Type Culture Collection (ATCC). The expressions of caspases 3, caspases 9, PARP, BAX, and BCL2 were detected by Western blot. Annexin V FITC, mitochondrial membrane potential, and reactive oxygen species were detected by flow cytometry. DAPI staining was detected by fluorescence microscopy. Cell viability was assessed by 3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide (MTT) assay. RESULTS We found that curcumin has cytotoxic activity in human glioma CHME cells, as shown by DAPI staining, annexin V/PI, and nuclear morphology. We found that cell growth decreased with increased concentration of curcumin, as well as sowing effects on expression of caspase-3, caspase-9, and cleavage of PARP, which suggests apoptotic cascade activity. The increase in reactive oxygen species and loss of mitochondrial membrane potential (Δψmt) in concentration-dependent manners suggests biochemical induction of apoptosis in CHME cells. CONCLUSIONS Curcumin has effective anticancer activity in human glioma CHME cells by inducing the apoptotic pathway.
作者机构：
[Xiao, Jianhua; Cao, Jingsong] Univ South China, Med Coll, Inst Pathogen Biol, Hunan Prov Key Lab Special Pathogens Prevent & Co, Hengyang 421001, Hunan, Peoples R China.;[Xiao, Jianhua; Cao, Jingsong] Univ South China, Hunan Prov Cooperat Innovat Ctr Mol Target New Dr, Hengyang 421001, Hunan, Peoples R China.;[Wang, Yi; Zhang, Yunsheng; Xiao, JH; Wang, Y; Xiao, Jianhua; Liu, Luogen; Cao, Jingsong] Univ South China, Affiliated Hosp 2, Inst Pathogen Biol, Clin Res Ctr,Med Coll, Hengyang 421001, Hunan, Peoples R China.;[Wang, Yi] Univ South China, Affiliated Hosp 2, Urinary Surg, Hengyang 421001, Hunan, Peoples R China.
通讯机构：
[Xiao, Jianhua; Xiao, JH; Wang, Y] U;Univ South China, Med Coll, Inst Pathogen Biol, Hunan Prov Key Lab Special Pathogens Prevent & Co, Hengyang 421001, Hunan, Peoples R China.;Univ South China, Hunan Prov Cooperat Innovat Ctr Mol Target New Dr, Hengyang 421001, Hunan, Peoples R China.;Univ South China, Affiliated Hosp 2, Inst Pathogen Biol, Clin Res Ctr,Med Coll, Hengyang 421001, Hunan, Peoples R China.
关键词：
Blood group B antigen;Blood group B antibody;HK2;B cells activation;ABOi-KT
摘要：
It is well known that ABO blood group system incompatible kidney transplantation (ABOi-KT) is an effective strategy for end-stage renal disease. The main barrier for ABOi-KT is how to keep host B cell activation and blood group antibody titer in low levels. Moreover, the mechanism of B cell activation induced by blood group antigen was unclear in ABOi-KT. In this study, HK2 cells were identified to express blood group B antigen when cocultured with lymphocytes of blood group A. Optical microscope observation demonstrated that HK2 cells in coculture group gradually decreased. Furthermore, flow cytometer assay identified that T cell phenotypes (CD3+, CD3+CD4+ and CD3+CD8+) had no significant change and B cell phenotypes (CD19+ and CD138+) were all significantly enhanced (3.07 and 3.02 folds) at day 4. In addition, immunoturbidimetry analysis demonstrated that blood group B antibody was significantly increased to 2.35 fold at day 4, IgG was significantly increased to 3.60 and 2.81 folds at days 4 and 8 respectively, while IgM had no significant change at the measured time points. Taken together, B cells were activated and secreted blood group B antibody after treatment with HK2 expressing blood group B antigen. The results of this study maybe useful for further determination of the mechanism of B cell activation after ABO incompatible kidney endothelial cells stimulation.
