2024 |
Zhang C, Jiang J-T, Guan Z, Zhang Y, Li Y, Song B, et al., 'Unveiling the sp
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2024 |
Tao H, Jin C, Zhou L, Deng Z, Li X, Dang W, et al., 'PRMT1 Inhibition Activates the Interferon Pathway to Potentiate Antitumor Immunity and Enhance Checkpoint Blockade Efficacy in Melanoma', CANCER RESEARCH, 84 419-433 (2024) [C1]
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2023 |
Zhang Y, Feng Y, Wu M, Deng Z, Wang S, 'VGAEDTI: drug-target interaction prediction based on variational inference and graph autoencoder', BMC BIOINFORMATICS, 24 (2023) [C1]
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2023 |
Zhang Y, Zhang X, Pang Q, Yan J, 'Control of metal oxides' electronic conductivity through visual intercalation chemical reactions', NATURE COMMUNICATIONS, 14 (2023) [C1]
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2023 |
Liu X, Zhang Y, Yang X, Zhang Y, Liu Y, Wang L, et al., 'Mitochondrial transplantation inhibits cholangiocarcinoma cells growth by balancing oxidative stress tolerance through PTEN/PI3K/AKT signaling pathway', TISSUE & CELL, 85 (2023) [C1]
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2023 |
Huang L, Liu B, Li L, Shi H, Xue Q, Zhang F, et al., 'Experimental Study on Performance Evaluation of Controlled Plasma Pulse Plugging Removal Technology', MACHINES, 11 (2023) [C1]
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2023 |
Zheng Y, Song W, Song Z, Zhang Y, Xin T, Liu C, et al., 'A Complicated Route from Disorder to Order in Antimony-Tellurium Binary Phase Change Materials', ADVANCED SCIENCE, [C1]
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2023 |
Zhang Y, Yan J, 'Recent advances in the synthesis of defective TiO
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2023 |
La T, Chen S, Zhao XH, Zhou S, Xu R, Teng L, et al., 'LncRNA LIMp27 Regulates the DNA Damage Response through p27 in p53-Defective Cancer Cells.', Adv Sci (Weinh), 10 e2204599 (2023) [C1]
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Nova |
2023 |
Tang D, Cai Q, Nie T, Zhang Y, Wu J, 'Agricultural price forecasting based on the spatial and temporal influences factors under spillover effects', KYBERNETES, [C1]
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2023 |
Jia W, Zhang Y, Wang X, Luo L, Sun H, Jiang Y, et al., 'KRT5 mutation regulate melanin metabolism through notch signalling pathway between keratinocytes and melanocytes', EXPERIMENTAL DERMATOLOGY, 32 752-765 (2023) [C1]
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2023 |
Fan X, Zhang Y, Song Y, Zhao Y, Xu Y, Guo F, et al., 'Compound Danshen Dripping Pills moderate intestinal flora and the TLR4/MyD88/NF-kappa B signaling pathway in alleviating cognitive dysfunction in type 2 diabetic KK-Ay mice', PHYTOMEDICINE, 111 (2023) [C1]
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2023 |
Zhang Y, Liu T, Deng Z, Fang W, Zhang X, Zhang S, et al., 'Group 2 Innate Lymphoid Cells Protect Mice from Abdominal Aortic Aneurysm Formation via IL5 and Eosinophils', ADVANCED SCIENCE, 10 (2023) [C1]
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2023 |
Li F, Huang X, Ma C, Xue J, Li Y, Kim D, et al., 'Tailoring the Interface with a Multifunctional Ligand for Highly Efficient and Stable FAPbI(3) Perovskite Solar Cells and Modules', ADVANCED SCIENCE, 10 (2023) [C1]
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2023 |
Zhou S, Liu L, Zhang Y, Zhang Z, Li H, Fan F, et al., 'Integrated untargeted and targeted metabolomics to reveal therapeutic effect and mechanism of Alpiniae oxyphyllae fructus on Alzheimer's disease in APP/PS1 mice', FRONTIERS IN PHARMACOLOGY, 13 (2023) [C1]
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2023 |
Ma H, Cui J, Liu Z, Fang W, Lu S, Cao S, et al., 'Blockade of de novo pyrimidine biosynthesis triggers autophagic degradation of oncoprotein FLT3-ITD in acute myeloid leukemia', ONCOGENE, 42 3331-3343 (2023) [C1]
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2022 |
Shang J, Cai X, Zhang T, Sun Y, Zhang Y, Liu J, Guan B, 'EpiReSIM: A Resampling Method of Epistatic Model without Marginal Effects Using Under-Determined System of Equations', GENES, 13 (2022)
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2022 |
Yang Y, Shang J, Sun Y, Li F, Zhang Y, Kong X-Z, et al., 'TLNPMD: Prediction of miRNA-Disease Associations Based on miRNA-Drug-Disease Three-Layer Heterogeneous Network', MOLECULES, 27 (2022)
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2022 |
Wang PL, Teng L, Feng YC, Yue YM, Han MM, Yan Q, et al., 'The N-Myc-responsive lncRNA MILIP promotes DNA double-strand break repair through non-homologous end joining', PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 119 (2022) [C1]
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Nova |
2021 |
Wang S, Liu G, Wang X, Zhang Y, He S, Zhang Y, 'TagSNP-set selection for genotyping using integrated data', FUTURE GENERATION COMPUTER SYSTEMS-THE INTERNATIONAL JOURNAL OF ESCIENCE, 115 327-334 (2021) [C1]
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2021 |
He Z, Zhang J, Yuan X, Zhang Y, 'Integrating Somatic Mutations for Breast Cancer Survival Prediction Using Machine Learning Methods', FRONTIERS IN GENETICS, 11 (2021) [C1]
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2021 |
Ding Q, Sun Y, Shang J, Li F, Zhang Y, Liu J-X, 'NMFNA: A Non-negative Matrix Factorization Network Analysis Method for Identifying Modules and Characteristic Genes of Pancreatic Cancer', FRONTIERS IN GENETICS, 12 (2021) [C1]
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2021 |
Shang J, Li Y, Sun Y, Li F, Zhang Y, Liu J-X, 'MOPIO: A Multi-Objective Pigeon-Inspired Optimization Algorithm for Community Detection', SYMMETRY-BASEL, 13 (2021) [C1]
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2021 |
Teng L, Feng YC, Guo ST, Wang PL, Qi TF, Yue YM, et al., 'The pan-cancer lncRNA PLANE regulates an alternative splicing program to promote cancer pathogenesis', NATURE COMMUNICATIONS, 12 (2021) [C1]
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Nova |
2021 |
La T, Chen S, Guo T, Zhao XH, Teng L, Li D, et al., 'Visualization of endogenous p27 and Ki67 reveals the importance of a c-Myc-driven metabolic switch in promoting survival of quiescent cancer cells', THERANOSTICS, 11 9605-9622 (2021) [C1]
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Nova |
2021 |
Sang B, Zhang YY, Guo ST, Kong LF, Cheng Q, Liu GZ, et al., 'Dual functions for OVAAL in initiation of RAF/MEK/ERK prosurvival signals and evasion of p27-mediated cellular senescence (vol 115, pg E11661, 2018)', PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 118 (2021)
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2020 |
Feng YC, Liu XY, Teng L, Ji Q, Wu Y, Li JM, et al., 'c-Myc inactivation of p53 through the pan-cancer lncRNA MILIP drives cancer pathogenesis', Nature Communications, 11 (2020) [C1]
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Nova |
2020 |
La T, Jin L, Liu XY, Song ZH, Farrelly M, Feng YC, et al., 'Cylindromatosis is required for survival of a subset of melanoma cells.', Oncology Research, 28 385-398 (2020) [C1]
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Nova |
2019 |
Yari H, Jin L, Teng L, Wang Y, Wu Y, Liu GZ, et al., 'LncRNA REG1CP promotes tumorigenesis through an enhancer complex to recruit FANCJ helicase for REG3A transcription', NATURE COMMUNICATIONS, 10 (2019) [C1]
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Nova |
2018 |
Sang B, Zhang YY, Guo ST, Kong LF, Cheng Q, Liu GZ, et al., 'Dual functions for OVAAL in initiation of RAF/MEK/ERK prosurvival signals and evasion of p27-mediated cellular senescence', Proceedings of the National Academy of Sciences of the United States of America, 115 E11661-E11670 (2018) [C1]
Long noncoding RNAs (lncRNAs) function through a diverse array of mechanisms that are not presently fully understood. Here, we sought to find lncRNAs differentially regulated in c... [more]
Long noncoding RNAs (lncRNAs) function through a diverse array of mechanisms that are not presently fully understood. Here, we sought to find lncRNAs differentially regulated in cancer cells resistant to either TNF-related apoptosis-inducing ligand (TRAIL) or the Mcl-1 inhibitor UMI-77, agents that act through the extrinsic and intrinsic apoptotic pathways, respectively. This work identified a commonly up-regulated lncRNA, ovarian adenocarcinoma-amplified lncRNA (OVAAL), that conferred apoptotic resistance in multiple cancer types. Analysis of clinical samples revealed OVAAL expression was significantly increased in colorectal cancers and melanoma in comparison to the corresponding normal tissues. Functional investigations showed that OVAAL depletion significantly inhibited cancer cell proliferation and retarded tumor xenograft growth. Mechanically, OVAAL physically interacted with serine/threonine-protein kinase 3 (STK3), which, in turn, enhanced the binding between STK3 and Raf-1. The ternary complex OVAAL/STK3/Raf-1 enhanced the activation of the RAF protooncogene serine/threonine-protein kinase (RAF)/mito-gen-activated protein kinase kinase 1 (MEK)/ERK signaling cascade, thus promoting c-Myc¿mediated cell proliferation and Mcl-1¿mediated cell survival. On the other hand, depletion of OVAAL triggered cellular senescence through polypyrimidine tract-binding protein 1 (PTBP1)¿mediated p27 expression, which was regulated by competitive binding between OVAAL and p27 mRNA to PTBP1. Additionally, c-Myc was demonstrated to drive OVAAL transcription, indicating a positive feedback loop between c-Myc and OVAAL in controlling tumor growth. Taken together, these results reveal that OVAAL contributes to the survival of cancer cells through dual mechanisms controlling RAF/MEK/ERK signaling and p27-mediated cell senescence.
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Nova |
2018 |
La T, Liu GZ, Farrelly M, Cole N, Feng YC, Zhang YY, et al., 'A p53-responsive miRNA network promotes cancer cell quiescence', Cancer Research, 78 6666-6679 (2018) [C1]
Cancer cells in quiescence (G0 phase) are resistant to death, and re-entry of quiescent cancer cells into the cell-cycle plays an important role in cancer recurrence. Here we show... [more]
Cancer cells in quiescence (G0 phase) are resistant to death, and re-entry of quiescent cancer cells into the cell-cycle plays an important role in cancer recurrence. Here we show that two p53-responsive miRNAs utilize distinct but complementary mechanisms to promote cancer cell quiescence by facilitating stabilization of p27. Purified quiescent B16 mouse melanoma cells expressed higher levels of miRNA-27b-3p and miRNA-455-3p relative to their proliferating counterparts. Induction of quiescence resulted in increased levels of these miRNAs in diverse types of human cancer cell lines. Inhibition of miRNA-27b-3p or miRNA-455-3p reduced, whereas its overexpression increased, the proportion of quiescent cells in the population, indicating that these miRNAs promote cancer cell quiescence. Accordingly, cancer xenografts bearing miRNA-27b-3p or miRNA-455-3p mimics were retarded in growth. miRNA-27b-3p targeted cyclin-dependent kinase regulatory subunit 1 (CKS1B), leading to reduction in p27 polyubiquitination mediated by S-phase kinase-associated protein 2 (Skp2). miRNA-455-3p targeted CDK2-associated cullin domain 1 (CAC1), which enhanced CDK2-mediated phosphorylation of p27 necessary for its polyubiquitination. Of note, the gene encoding miRNA-27b-3p was embedded in the intron of the chromosome 9 open reading frame 3 gene that was transcriptionally activated by p53. Similarly, the host gene of miRNA-455-3p, collagen alpha-1 (XXVII) chain, was also a p53 transcriptional target. Collectively, our results identify miRNA-27b-3p and miRNA-455-3p as important regulators of cancer cell quiescence in response to p53 and suggest that manipulating miRNA-27b-3p and miRNA-455-3p may constitute novel therapeutic avenues for improving outcomes of cancer treatment. Significance: Two novel p53-responsive microRNAs whose distinct mechanisms of action both stabilize p27 to promote cell quiescence and may serve as therapeutic avenues for improving outcomes of cancer treatment.
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Nova |
2018 |
Zhang YY, Tabataba H, Liu XY, Wang JY, Yan XG, Farrelly M, et al., 'ACTN4 regulates the stability of RIPK1 in melanoma', ONCOGENE, 37 4033-4045 (2018) [C1]
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Nova |
2017 |
Liu F, Jiang CC, Yan XG, Tseng H-Y, Wang CY, Zhang YY, et al., 'BRAF/MEK inhibitors promote CD47 expression that is reversible by ERK inhibition in melanoma.', Oncotarget, 8 69477-69492 (2017) [C1]
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Nova |
2016 |
Yanwang C, Guo ST, Yuwang J, Liu F, Zhang YY, Yari H, et al., 'Inhibition of HSP90 by AUY922 preferentially kills mutantkrascolon cancer cellsbyactivatingbim through ER stress', Molecular Cancer Therapeutics, 15 448-459 (2016) [C1]
Oncogenic mutations of KRAS pose a great challenge in the treatment of colorectal cancer. Here we report that mutant KRAS colon cancer cells are nevertheless more susceptible to a... [more]
Oncogenic mutations of KRAS pose a great challenge in the treatment of colorectal cancer. Here we report that mutant KRAS colon cancer cells are nevertheless more susceptible to apoptosis induced by the HSP90 inhibitor AUY922 than those carrying wild-type KRAS. Although AUY922 inhibited HSP90 activity with comparable potency in colon cancer cells irrespective of their KRAS mutational statuses, those with mutant KRAS were markedly more sensitive to AUY922-induced apoptosis. This was associated with upregulation of the BH3-only proteins Bim, Bik, and PUMA.However, only Bim appeared essential, in that knockdown of Bim abolished, whereas knockdown of Bik or PUMA only moderately attenuated apoptosis induced by AUY922. Mechanistic investigations revealed that endoplasmic reticulum (ER) stress was responsible for AUY922-induced upregulation of Bim, which was inhibited by a chemical chaperone or overexpression of GRP78. Conversely, siRNA knockdown of GRP78 or XBP-1 enhanced AUY922-induced apoptosis. Remarkably, AUY922 inhibited the growth of mutant KRAS colon cancer xenografts through activation of Bim that was similarly associated with ER stress. Taken together, these results suggest that AUY922 is a promising drug in the treatment of mutant KRAS colon cancers, and the agents that enhance the apoptosis-inducing potential of Bimmaybe useful to improve the therapeutic efficacy.
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Nova |
2016 |
Wang JY, Jin L, Yan XG, Sherwin S, Farrelly M, Zhang YY, et al., 'Reactive Oxygen Species Dictate the Apoptotic Response of Melanoma Cells to TH588', Journal of Investigative Dermatology, 136 2277-2286 (2016) [C1]
The effect of MTH1 inhibition on cancer cell survival has been elusive. Here we report that although silencing of MTH1 does not affect survival of melanoma cells, TH588, one of th... [more]
The effect of MTH1 inhibition on cancer cell survival has been elusive. Here we report that although silencing of MTH1 does not affect survival of melanoma cells, TH588, one of the first-in-class MTH1 inhibitors, kills melanoma cells through apoptosis independently of its inhibitory effect on MTH1. Induction of apoptosis by TH588 was not alleviated by MTH1 overexpression or introduction of the bacterial homolog of MTH1 that has 8-oxodGTPase activity but cannot be inhibited by TH588, indicating that MTH1 inhibition is not the cause of TH588-induced killing of melanoma cells. Although knockdown of MTH1 did not impinge on the viability of melanoma cells, it rendered melanoma cells sensitive to apoptosis induced by the oxidative stress inducer elesclomol. Of note, treatment with elesclomol also enhanced TH588-induced apoptosis, whereas a reactive oxygen species scavenger or an antioxidant attenuated the apoptosis triggered by TH588. Indeed, the sensitivity of melanoma cells to TH588 was correlated with endogenous levels of reactive oxygen species. Collectively, these results indicate that the cytotoxicity of TH588 toward melanoma cells is not associated with its inhibitory effect on MTH1, although it is mediated by cellular production of ROS.
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Nova |
2016 |
Wang CY, Guo ST, Wang JY, Yan XG, Farrelly M, Zhang YY, et al., 'Reactivation of ERK and Akt confers resistance of mutant BRAF colon cancer cells to the HSP90 inhibitor AUY922', Oncotarget, 7 49597-49610 (2016) [C1]
Oncogenic mutations of BRAF occur in approximately 10% of colon cancers and are associated with their resistance to clinically available therapeutic drugs and poor prognosis of th... [more]
Oncogenic mutations of BRAF occur in approximately 10% of colon cancers and are associated with their resistance to clinically available therapeutic drugs and poor prognosis of the patients. Here we report that colon cancer cells with mutant BRAF are also resistant to the heat shock protein 90 (HSP90) inhibitor AUY922, and that this is caused by rebound activation of ERK and Akt. Although AUY922 triggered rapid reduction in ERK and Akt activation in both wild-type and mutant BRAF colon cancer cells, activation of ERK and Akt rebounded shortly in the latter leading to resistance of the cells to AUY922-induced apoptosis. Reactivation of ERK was associated with the persistent expression of mutant BRAF, which, despite being a client of HSP90, was only partially degraded by AUY922, whereas reactivation of Akt was related to the activity of the HSP90 co-chaperone, cell division cycle 37 (CDC37), in that knockdown of CDC37 inhibited Akt reactivation in mutant colon cancer cells treated with AUY922. In support, as a HSP90 client protein, Akt was only diminished by AUY922 in wild-type but not mutant BRAF colon cancer cells. Collectively, these results reveal that reactivation of ERK and Akt associated respectively with the activity of mutant BRAF and CDC37 renders mutant BRAF colon cancer cells resistant to AUY922, with implications of co-targeting mutant BRAF and/or CDC37 and HSP90 in the treatment of mutant BRAF colon cancers.
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Nova |
2014 |
Zhang Q, Zhang Y, Zhang P, Chao Z, Xia F, Jiang C, et al., 'Hexokinase II inhibitor, 3-BrPA induced autophagy by stimulating ROS formation in human breast cancer cells', Genes and Cancer, 5 100-112 (2014)
Hexokinase II (HKII), a key enzyme of glycolysis, is widely over-expressed in cancer cells. 3-bromopyruvate (3-BrPA), an inhibitor of HK II, has been proposed as a specific antitu... [more]
Hexokinase II (HKII), a key enzyme of glycolysis, is widely over-expressed in cancer cells. 3-bromopyruvate (3-BrPA), an inhibitor of HK II, has been proposed as a specific antitumor agent. Autophagy is a process that regulates the balance between protein synthesis and protein degradation. Autophagy in mammalian systems occurs under basal conditions and can be stimulated by stresses, including starvation, oxidative stress. Therefore, we hypothesized that 3-BrPA could induce autophagy. In the present study, we explored the mechanism of 3-BrPA and its combined action with chloroquine. Our results demonstrate that in MDA-MB-435 and in MDA-MB-231 cells, 3-BrPA induces autophagy, which can be inhibited by chloroquine. Furthermore, the combined treatment synergistically decreased the number of viable cells. Interestingly, the combined treatment triggered apoptosis in MDA-MB-435 cells, while it induced necroptosis in MDA-MB-231 cells. ROS mediated cell death when 3-BrPA and CQ were co-administered. Finally, CQ enhanced the anticancer efficacy of 3-BrPA in vivo. Collectively, our results show that 3-BrPA triggers autophagy, increasing breast cancer cell resistance to 3-BrPA treatment and that CQ enhanced 3-BrPA-induced cell death in breast cancer cells by stimulating ROS formation. Thus, inhibition of autophagy may be an innovative strategy for adjuvant chemotherapy of breast cancer
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2014 |
Zhao RS, Zhang YY, Wu CZ, Li HM, Jiang C, Jiang ZW, Liu H, '3-bromopyruvate enhances cisplatin sensitivity of hepatocellular carcinoma cells in vitro.', Nan Fang Yi Ke Da Xue Xue Bao = Journal of Southern Medical University, 34 25-30 (2014) [C1]
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Nova |
2014 |
Liu Z, Zhang Y-Y, Zhang Q-W, Zhao S-R, Wu C-Z, Cheng X, et al., '3-Bromopyruvate induces apoptosis in breast cancer cells by downregulating Mcl-1 through the PI3K/Akt signaling pathway', ANTI-CANCER DRUGS, 25 447-455 (2014) [C1]
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Nova |
2014 |
Zhang P, Liu H, Xia F, Zhang QW, Zhang YY, Zhao Q, et al., 'Epithelial-mesenchymal transition is necessary for acquired resistance to cisplatin and increases the metastatic potential of nasopharyngeal carcinoma cells', INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE, 33 151-159 (2014) [C1]
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Nova |
2013 |
Xu JC, Xia F, Zhang P, Pu LJ, Huang YY, Li Y, et al., 'Effect of tunicamycin combined with oxaliplatin on proliferation and apoptosis of human oral squamous carcinoma cells in vitro', Chinese Pharmacological Bulletin, 29 956-961 (2013)
Aim: To study the effects of tunicamycin combined with oxaliplatin on the proliferation and apoptosis of human oral cancer cells and its related molecular mechanism. Methods: MTT ... [more]
Aim: To study the effects of tunicamycin combined with oxaliplatin on the proliferation and apoptosis of human oral cancer cells and its related molecular mechanism. Methods: MTT method was applied to detect the drug to the influence of cell proliferation inhibition; colony clone formation method was used to detect the drug to cell colony clone formation of influence; the cell apoptosis was analyzed using flow cytometry with propidium iodide staining. Caspase-3 active detection kit was employed for detection of the drug effect within 24 h on Caspase-3 activity change; Western blot was applied to test Caspase-3, Caspase-12 protein expression and protein expression of glucose regulation 78. Results: The different concentrations of tunicamycin and/or oxaliplatin had significant proliferation inhibition on oral cancer KB cells (The cell survival rate of 0.125 µmol·L-1 tunicamycin administered in oral cancer KB cells after 24, 48, 72 h was 90.37%, 89.44% and 88.91% respectively), While that of 0.125 µmol·L-1 tunicamycin combined with 1 µmol·L-1 oxaliplatin applied in oral cancer KB cells after 24, 48, 72 h was lower than that of the single dose of tunicamycin or oxaliplatin. The survival rate of three groups was 50.78%, 37.77%, 23.24%, respectively. 0.25 µmol·L-1 tunicamycin can enhance the action of oxaliplatin on oral cancer cells KB colony clone formation. The apoptotic rate of 0.5 µmol·L-1 tunicamycin induced KB cells after 48 h was 8.3%, and that of 0.5 µmol·L-1 tunicamycin and 1 µmol·L-1 oxaliplatin stimulating human oral cancer cells KB after 48 h was 50.3%, Which was higher than the apoptotic rate of 24.6% incuced only by oxaliplatin. Tunicamycin could raise GRP-78 expression and enhance Caspase-3 activity and expression in combined treatment group. Conclusion: Tunicamycin can enhance the proliferation inhibition and apoptosis inducement caused by oxaliplatin in oral cancer cells, and the mechanism may be caused by excessive endoplasmic reticulum stress reaction and increase of Caspase-3 activity.
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2013 |
Zhang QW, Zhang YY, Zhao ZH, Zhang P, Jiang CC, Liu H, Jiang ZW, 'Influence of hydroxychloroquine on the proliferation and apoptosis of breast cancer cell MDA-MB-435', Chinese Pharmacological Bulletin, 29 1549-1553 (2013)
Aim: To observe the influence of hydroxychloroquine (HCQ) on the proliferation and apoptosis of breast cancer cell MDA-MB-435. Methods: The effect of HCQ on the proliferation of M... [more]
Aim: To observe the influence of hydroxychloroquine (HCQ) on the proliferation and apoptosis of breast cancer cell MDA-MB-435. Methods: The effect of HCQ on the proliferation of MDA-MB-435 cell was evaluated by MTT assay and clone formation assay; morphological changes of MDA-MB-435 cell after HCQ treatment was observed by inverted microscope; Hoechst 33258 staining was used to assess the changes in HCQ-induced apoptosis of MDA-MB-435 cell; PI staining was used to analyze the apoptosis of the cell exposed to HCQ; JC-1 was used to detect the changes of mitochondrial membrane potential of MDA-MB-435 cell. Results: Incubation with HCQ for 24 h, 48 h and 72 h resulted in a significant inhibition of MDA-MB-435 cell proliferation; HCQ treatment at different concentrations caused MDA-MB-435 cell turning round and shrinkage gradually, density of cell turning smaller gradually and losing the normal cell morphology; HCQ treatment also inhibited cell colony formation; Hoechst 33258 staining showed HCQ could induce apoptosis of MDA-MB-435 cell; exposure to 20, 40, 60 µmol · L-1HCQ for 24 h caused a percentage of late apoptotic cells of 7.1%, 15.9%, 35.3% (P < 0.05); HCQ treatment at different concentrations also turned JC-1 from red to green (P < 0.05). Conclusion: HCQ can significantly inhibit the proliferation of MDA-MB-435 cell and induce apoptosis.
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2013 |
Zhang Y-Y, Liu H, 'Connections Between Various Trigger Factors and the RIP1/RIP3 Signaling Pathway Involved in Necroptosis', ASIAN PACIFIC JOURNAL OF CANCER PREVENTION, 14 7069-7074 (2013)
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