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19 results on '"Tang, ChangYan"'

5. Genome-wide association studies reveal the role of polymorphisms affecting factor H binding protein expression in host invasion by Neisseria meningitidis

Author

Earle, Sarah G., primary, Lobanovska, Mariya, additional, Lavender, Hayley, additional, Tang, Changyan, additional, Exley, Rachel M., additional, Ramos-Sevillano, Elisa, additional, Browning, Douglas F., additional, Kostiou, Vasiliki, additional, Harrison, Odile B., additional, Bratcher, Holly B., additional, Varani, Gabriele, additional, Tang, Christoph M., additional, Wilson, Daniel J., additional, and Maiden, Martin C. J., additional

Published
2021
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7. Polymorphisms affecting expression of the vaccine antigen factor H binding protein influence invasiveness of Neisseria meningitidis

Author

Earle, Sarah G., primary, Lobanovska, Mariya, additional, Lavender, Hayley, additional, Tang, Changyan, additional, Exley, Rachel M., additional, Ramos-Sevillano, Elisa, additional, Browning, Douglas, additional, Kostiou, Vasiliki, additional, Harrison, Odile B., additional, Bratcher, Holly B., additional, Varani, Gabriele, additional, Tang, Christoph M., additional, Wilson, Daniel J., additional, and Maiden, Martin C. J., additional

Published
2021
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8. The Long Noncoding RNA CCAT2 Induces Chromosomal Instability Through BOP1-AURKB Signaling

Author

Chen, Baoqing, primary, Dragomir, Mihnea P., additional, Fabris, Linda, additional, Bayraktar, Recep, additional, Knutsen, Erik, additional, Liu, Xu, additional, Tang, Changyan, additional, Li, Yongfeng, additional, Shimura, Tadanobu, additional, Ivkovic, Tina Catela, additional, Cruz De los Santos, Mireia, additional, Anfossi, Simone, additional, Shimizu, Masayoshi, additional, Shah, Maitri Y., additional, Ling, Hui, additional, Shen, Peng, additional, Multani, Asha S., additional, Pardini, Barbara, additional, Burks, Jared K., additional, Katayama, Hiroyuki, additional, Reineke, Lucas C., additional, Huo, Longfei, additional, Syed, Muddassir, additional, Song, Shumei, additional, Ferracin, Manuela, additional, Oki, Eiji, additional, Fromm, Bastian, additional, Ivan, Cristina, additional, Bhuvaneshwar, Krithika, additional, Gusev, Yuriy, additional, Mimori, Koshi, additional, Menter, David, additional, Sen, Subrata, additional, Matsuyama, Takatoshi, additional, Uetake, Hiroyuki, additional, Vasilescu, Catalin, additional, Kopetz, Scott, additional, Parker-Thornburg, Jan, additional, Taguchi, Ayumu, additional, Hanash, Samir M., additional, Girnita, Leonard, additional, Slaby, Ondrej, additional, Goel, Ajay, additional, Varani, Gabriele, additional, Gagea, Mihai, additional, Li, Chunlai, additional, Ajani, Jaffer A., additional, and Calin, George A., additional

Published
2020
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18. NF-κB, JNK and p53 pathways are involved in tubeimoside-1-induced apoptosis in HepG2 cells with oxidative stress and G2/M cell cycle arrest

Author

Yin, Yan, Chen, Wei, Tang, Changyan, Ding, Hanjing, Jang, Jongchol, Weng, Meizhi, Cai, Yongjun, and Zou, Guolin

Subjects
*NF-kappa B, *APOPTOSIS, *TERPENES, *HERBAL medicine, *CELL cycle, *OXIDATIVE stress, *SAPONINS
Abstract

Abstract: Tubeimoside-1 is a triterpenoid saponin extracted from the traditional Chinese herb Bolbostemma paniculatum (Maxim.) Franquet (Cucurbitaceae). We investigated the cytotoxic effect and apoptosis mechanism of tubeimoside-1. Tubeimoside-1 was cytotoxic in seven human cancer cell lines, with HepG2 the most sensitive. Tubeimoside-1 induced apoptosis of HepG2 cells dose and time dependently. Both the extrinsic and intrinsic pathways were triggered by tubeimoside-1. Caspase-3, -8 and -9 were activated and the expression of Fas, Fas ligand, Bcl-2, Bak and Bax was regulated. Moreover, tubeimoside-1 induced accumulation of reactive oxygen species and arrested cell cycle at the G2/M phase, thus contributing to apoptosis, through signaling regulation by tumor necrosis factor α, nuclear factor κB (NF-κB), Jun N-terminal kinase (JNK) and p53. We provide further insight into the tubeimoside-1 cytotoxic effect for antitumor chemotherapeutic treatment. [Copyright &y& Elsevier]

Published
2011
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19. The Long Noncoding RNA CCAT2 Induces Chromosomal Instability Through BOP1-AURKB Signaling

Author

Mihai Gagea, Eiji Oki, Manuela Ferracin, Recep Bayraktar, Scott Kopetz, Peng Shen, Hiroyuki Uetake, Masayoshi Shimizu, Cristina Ivan, Mireia Cruz De los Santos, Samir M. Hanash, Barbara Pardini, Bastian Fromm, Gabriele Varani, Longfei Huo, Xu Liu, Maitri Y. Shah, Jaffer A. Ajani, Mihnea P. Dragomir, David G. Menter, Jan Parker-Thornburg, Tadanobu Shimura, Koshi Mimori, Chunlai Li, Jared K. Burks, Subrata Sen, Catalin Vasilescu, Simone Anfossi, Erik Knutsen, Yuriy Gusev, Yongfeng Li, Shumei Song, Krithika Bhuvaneshwar, Ondrej Slaby, Tina Catela Ivkovic, Asha S. Multani, Lucas C. Reineke, Linda Fabris, Muddassir Syed, Hui Ling, Ajay Goel, Ayumu Taguchi, Baoqing Chen, George A. Calin, Leonard Girnita, Changyan Tang, Takatoshi Matsuyama, Hiroyuki Katayama, Chen, Baoqing, Dragomir, Mihnea P, Fabris, Linda, Bayraktar, Recep, Knutsen, Erik, Liu, Xu, Tang, Changyan, Li, Yongfeng, Shimura, Tadanobu, Ivkovic, Tina Catela, Cruz De Los Santos, Mireia, Anfossi, Simone, Shimizu, Masayoshi, Shah, Maitri Y, Ling, Hui, Shen, Peng, Multani, Asha S, Pardini, Barbara, Burks, Jared K, Katayama, Hiroyuki, Reineke, Lucas C, Huo, Longfei, Syed, Muddassir, Song, Shumei, Ferracin, Manuela, Oki, Eiji, Fromm, Bastian, Ivan, Cristina, Bhuvaneshwar, Krithika, Gusev, Yuriy, Mimori, Koshi, Menter, David, Sen, Subrata, Matsuyama, Takatoshi, Uetake, Hiroyuki, Vasilescu, Catalin, Kopetz, Scott, Parker-Thornburg, Jan, Taguchi, Ayumu, Hanash, Samir M, Girnita, Leonard, Slaby, Ondrej, Goel, Ajay, Varani, Gabriele, Gagea, Mihai, Li, Chunlai, Ajani, Jaffer A, and Calin, George A

Subjects
Male, 0301 basic medicine, Small interfering RNA, Carcinogenesis, medicine.disease_cause, Noncoding RNA, Mice, chemistry.chemical_compound, 0302 clinical medicine, Aurora kinase, Chromosome instability, Antineoplastic Combined Chemotherapy Protocols, Gene expression, Aurora Kinase B, Intestinal Mucosa, Gene knockdown, Gastroenterology, RNA-Binding Proteins, Dextrans, 3. Good health, Gene Expression Regulation, Neoplastic, Organoids, Gene Knockdown Techniques, Cytogenetic Analysis, Female, RNA, Long Noncoding, 030211 gastroenterology & hepatology, Colorectal Neoplasms, Signal Transduction, Colon, Transgene, Primary Cell Culture, Azoxymethane, Mice, Transgenic, Biology, Article, Proto-Oncogene Proteins c-myc, 03 medical and health sciences, Cell Line, Tumor, Chromosomal Instability, medicine, Animals, Humans, MSS, Hepatology, Neoplasms, Experimental, Aneuploidy, Tumorigenesis, digestive system diseases, 030104 developmental biology, chemistry, Drug Resistance, Neoplasm, Cancer research
Abstract

BACKGROUND & AIMS: Chromosomal instability (CIN) is a carcinogenesis event that promotes metastasis and resistance to therapy by unclear mechanisms. Expression of the colon cancer-associated transcript 2 gene (CCAT2), which encodes a long noncoding RNA (lncRNA), associates with CIN, but little is known about how CCAT2 lncRNA regulates this cancer enabling characteristic.METHODS: We performed cytogenetic analysis of colorectal cancer (CRC) cell lines (HCT116, KM12C/SM, and HT29) overexpressing CCAT2 and colon organoids from C57BL/6N mice with the CCAT2 transgene and without (controls). CRC cells were also analyzed by immunofluorescence microscopy, gamma-H2AX, and senescence assays. CCAT2 transgene and control mice were given azoxymethane and dextran sulfate sodium to induce colon tumors. We performed gene expression array and mass spectrometry to detect downstream targets of CCAT2 lncRNA. We characterized interactions between CCAT2 with downstream proteins using MS2 pull-down, RNA immunoprecipitation, and selective 2'-hydroxyl acylation analyzed by primer extension analyses. Downstream proteins were overexpressed in CRC cells and analyzed for CIN. Gene expression levels were measured in CRC and non-tumor tissues from 5 cohorts, comprising more than 900 patients.RESULTS: High expression of CCAT2 induced CIN in CRC cell lines and increased resistance to 5-fluorouracil and oxaliplatin. Mice that expressed the CCAT2 transgene developed chromosome abnormalities, and colon organoids derived from crypt cells of these mice had a higher percentage of chromosome abnormalities compared with organoids from control mice. The transgenic mice given azoxymethane and dextran sulfate sodium developed more and larger colon polyps than control mice given these agents. Microarray analysis and mass spectrometry indicated that expression of CCAT2 increased expression of genes involved in ribosome biogenesis and protein synthesis. CCAT2 lncRNA interacted directly with and stabilized BOP1 ribosomal biogenesis factor (BOP1). CCAT2 also increased expression of MYC, which activated expression of BOP1. Overexpression of BOP1 in CRC cell lines resulted in chromosomal missegregation errors, and increased colony formation, and invasiveness, whereas BOP1 knockdown reduced viability. BOP1 promoted CIN by increasing the active form of aurora kinase B, which regulates chromosomal segregation. BOP1 was overexpressed in polyp tissues from CCAT2 transgenic mice compared with healthy tissue. CCAT2 lncRNA and BOP1 mRNA or protein were all increased in microsatellite stable tumors (characterized by CIN), but not in tumors with microsatellite instability compared with nontumor tissues. Increased levels of CCAT2 lncRNA and BOP1 mRNA correlated with each other and with shorter survival times of patients.CONCLUSIONS: We found that overexpression of CCAT2 in colon cells promotes CIN and carcinogenesis by stabilizing and inducing expression of BOP1 an activator of aurora kinase B. Strategies to target this pathway might be developed for treatment of patients with microsatellite stable colorectal tumors.

Published
2020

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