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4 results on '"Ren JZ"'

1. [Corrigendum] SMC1A promotes growth and migration of prostate cancer in vitro and in vivo .

Author

Pan XW, Gan SS, Ye JQ, Fan YH, Hong Y, Chu CM, Gao Y, Li L, Liu X, Chen L, Huang Y, Xu H, Ren JZ, Yin L, Qu FJ, Huang H, Cui XG, and Xu DF

Abstract

Subsequently to the publication of the above article, an interested reader drew to the authors' attention that, on p. 1969, two pairs of panels shown for the DU145 data appeared to contain overlaps, such that they may have been derived from the same original source (specifically, relating to the shCon and the shSMC1A experiments). The authors have referred back to their original data, and realize that inadvertent errors were made during the assembly of these figures. The corrected version of Fig. 5, showing discrete representative images for the shCon and the shSMC1A experiments with the DU145 cell line, is shown on the next page. All the authors agree to this corrigendum. Note that the revisions made to this figure do not adversely affect the results reported in the paper, or the conclusions stated therein. The authors regret that Fig. 5 was not presented in its correct form in their paper, thank the Editor of International Journal of Oncology for granting them the opportunity to publish this corrigendum, and offer their apologies to the Editor and to the readers of the Journal. [the original article was published in International Journal of Oncology 49: 1963-1972, 2016; DOI: 10.3892/ijo.2016.3697].

Published
2021
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2. Quercetin nanoparticles display antitumor activity via proliferation inhibition and apoptosis induction in liver cancer cells.

Author

Ren KW, Li YH, Wu G, Ren JZ, Lu HB, Li ZM, and Han XW

Subjects
Antioxidants administration & dosage, Antioxidants adverse effects, Autophagy, Caspase 3 metabolism, Caspase 9 metabolism, Cell Line, Tumor, Cell Movement, Cyclooxygenase 2 metabolism, Cytochromes c metabolism, Drug Delivery Systems, Gold chemistry, Humans, MAP Kinase Signaling System, NF-kappa B metabolism, Nanoparticles chemistry, Promoter Regions, Genetic, Proto-Oncogene Proteins c-akt metabolism, Quercetin administration & dosage, Quercetin adverse effects, Telomerase metabolism, Transcription Factor AP-2 metabolism, Antioxidants therapeutic use, Apoptosis drug effects, Carcinoma, Hepatocellular drug therapy, Cell Proliferation drug effects, Liver Neoplasms drug therapy, Quercetin therapeutic use
Abstract

Quercetin is a potent cancer therapeutic agent and dietary antioxidant present in fruit and vegetables. Quercetin prevents tumor proliferation by inducing cell cycle arrest and is a well known cancer therapeutic agent and autophagy mediator. Recent studies showed that drug delivery by nanoparticles have enhanced efficacy with reduced side effects. In this regard, gold-quercetin into poly(DL-lactide-co-glycolide) nanoparticles was examined. In this study, we explored the role and possible underlying mechanisms of quercetin nanoparticle in regulation of antitumor activity in liver cancer cells. Treatment with quercetin nanoparticle effectively inhibited the liver cancer cell proliferation, cell migration and colony formation, thus suppressing liver cancer progression. Quercetin nanoparticle also upregulated apoptosis markedly. Further study suggested that quercetin nanoparticle accelerated the cleavage of caspase-9, caspase-3, and induced the up-releasing of cytochrome c (Cyto-c), contributing to apoptosis in liver cancer cells. Quercetin nanoparticles also promoted telomerase reverse transcriptase (hTERT) inhibition through reducing AP-2β expression and decreasing its binding to hTERT promoter. In addition, quercetin nanoparticle had an inhibitory role in cyclooxygenase 2 (COX-2) via suppressing the NF-κB nuclear translocation and its binding to COX-2 promoter. Quercetin nanoparticle also inactivated Akt and ERK1/2 signaling pathway. Taken together, our results suggested that quercetin nanoparticle had an antitumor effect by inactivating caspase/Cyto-c pathway, suppressing AP-2β/hTERT, inhibiting NF-κB/COX-2 and impeding Akt/ERK1/2 signaling pathways. Our results provided new mechanistic basis for further investigation of quercetin nanoparticles to find potential therapeutic strategies and possible targets for liver cancer inhibition.

Published
2017
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3. SMC1A promotes growth and migration of prostate cancer in vitro and in vivo.

Author

Pan XW, Gan SS, Ye JQ, Fan YH, Hong Υ, Chu CM, Gao Y, Li L, Liu X, Chen L, Huang Y, Xu H, Ren JZ, Yin L, Qu FJ, Huang H, Cui XG, and Xu DF

Subjects
Animals, Apoptosis, Biomarkers, Tumor genetics, Blotting, Western, Cell Cycle Proteins genetics, Chromosomal Proteins, Non-Histone genetics, Flow Cytometry, Humans, Immunoenzyme Techniques, In Vitro Techniques, Male, Mice, Mice, Inbred BALB C, Mice, Nude, Neoplasm Recurrence, Local genetics, Neoplasm Recurrence, Local metabolism, Neoplasm Staging, Prognosis, Prostatic Neoplasms genetics, Prostatic Neoplasms metabolism, RNA, Messenger genetics, Real-Time Polymerase Chain Reaction, Reverse Transcriptase Polymerase Chain Reaction, Tumor Cells, Cultured, Xenograft Model Antitumor Assays, Biomarkers, Tumor metabolism, Cell Cycle Proteins metabolism, Cell Movement, Cell Proliferation, Chromosomal Proteins, Non-Histone metabolism, Neoplasm Recurrence, Local pathology, Prostatic Neoplasms pathology
Abstract

Structural maintenance of chromosome 1 alpha (SMC1A) gene has been reported to be related to tumor development in some types of human cancers. However, the misregulation of SMC1A and its functions in castration-resistant prostate cancer (CRPC) have not been well understood. In the present study, we found that SMC1A was elevated in androgen-independent PCa cell lines PC-3 and DU-145 compared to androgen sensitive LNCap and 22RV1 cells by qPCR and western blot assay. Knockdown of SMC1A inhibited cell growth, colony formation and cell migration abilities of PC-3 and DU145 cells by MTT, colony formation and transwell assays, and affected cell cycle progression in PC-3 and DU145 cells by flow cytometry. Moreover, SMC1A knockdown significantly reduced tumor growth in vivo in a nude mouse model. Additionally, we also found that the expression of SMC1A gene was higher in prostate cancer tissues than in the adjacent normal tissues by immunohistochemical staining, and was positively correlated to tumor metastasis and recurrence by Oncomine database mining. Taken together, the present study indicates that SMC1A may play an important role in malignant transformation of PCa under conditions of androgen deprivation and act as a new target for PCa diagnosis and treatment.

Published
2016
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4. Icaritin acts synergistically with epirubicin to suppress bladder cancer growth through inhibition of autophagy.

Author

Pan XW, Li L, Huang Y, Huang H, Xu DF, Gao Y, Chen L, Ren JZ, Cao JW, Hong Y, and Cui XG

Subjects
Cell Line, Tumor, Cell Proliferation drug effects, Cell Survival drug effects, Dose-Response Relationship, Drug, Drug Resistance, Neoplasm drug effects, Drug Synergism, HEK293 Cells, Humans, Membrane Potential, Mitochondrial drug effects, Time Factors, Urinary Bladder Neoplasms drug therapy, Autophagy drug effects, Epirubicin pharmacology, Flavonoids pharmacology, Urinary Bladder Neoplasms metabolism
Abstract

Bladder cancer is one of the most commonly diagnosed urological malignancies. Acquired resistance to chemotherapy is a great barrier for achieving successful treatment of bladder cancer. In the present study, we investigated the effect and mechanisms of icaritin, a flavonol glycoside derived from genus Epimedium, against human bladder cancer cells. It was found that despite the low cytotoxicity in normal human HEK293 cells, icaritin significantly inhibited the proliferation and colony formation of BT5637 and T24 bladder cancer cells time- and dose-dependently compared to the DMSO vehicle control. Moreover, cell viability monitored through mitochondrial membrane potential was inhibited markedly after icaritin treatment. Further investigation indicated that icaritin may inhibit epirubicin (EPI)-induced autophagy, and acted synergistically with EPI to suppress the proliferation of BT5637 and T24 cells. These findings suggest that icaritin may prove to be a novel potent therapeutic agent for the treatment of bladder cancer.

Published
2016
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