RESUMEN
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the GAPDH control western blotting data shown in Fig. 1C were strikingly similar to data appearing in different form in another article written by different authors at different research institutes [Chen Y, Guo Y, Yang H, Shi G, Xu G, Shi J, Yin N and Chen D: TRIM66 overexpression contributes to osteosarcoma carcinogenesis and indicates poor survival outcome. Oncotarget 6: 2370823719, 2015]. Moreover, a pair of data panels showing the results from cellcycle experiments purportedly performed under different experimental conditions in Fig. 4A appeared to be strikingly similar. Owing to the fact that the contentious data in the above article were already under consideration for publication prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 14: 15231530, 2016; DOI: 10.3892/mmr.2016.5401].
RESUMEN
Cyclin-dependent kinase inhibitor 3 (CDKN3) belongs to the dual-specificity protein phosphatase family, which is hypothesized to regulate cell cycle progression in tumor cells. However, whether CDKN3 is a potential therapeutic target for breast cancer remains to be elucidated. The present in vitro study aimed to investigate the potential roles of CDKN3 in breast cancer. Breast cancer cell lines were used to detect CDKN3 expression, and CDKN3 expression was silenced to investigate its role in cell apoptosis, cell cycle arrest and migration. The underlying mechanisms were screened by detecting proliferating cell nuclear antigen (PCNA), Ras homolog gene family, member A (RhoA), vimentin, Bcell lymphoma 2 (Bcl2) and Bcl2associated X protein (Bax) expression. CDKN3 was highly expressed in MCF7 and BT474 cell lines. The silencing of CDKN3 in MCF7 and BT474 cell lines promoted cell apoptosis, induced G1 phase cell cycle arrest and inhibited cell migration. The expression levels of PCNA, RhoA, vimentin and Bcl2 were downregulated following CDKN3 silencing. Conversely, Bax expression was increased, as compared with the vehicle control. These results suggest that CDKN3 acts as an oncogene during breast cancer progression. The in vitro silencing of CDKN3 promoted apoptosis, induced G1 phase cell cycle arrest and inhibited cell migration. Possible mechanisms are associated with the regulation of PCNA, Bcl2, vimentin, RhoA and Bax expression. CDKN3 may therefore be considered a potential target for the treatment of breast cancer.
Asunto(s)
Neoplasias de la Mama/genética , Movimiento Celular/genética , Proteínas Inhibidoras de las Quinasas Dependientes de la Ciclina/genética , Fosfatasas de Especificidad Dual/genética , Silenciador del Gen , Apoptosis/genética , Neoplasias de la Mama/patología , Puntos de Control del Ciclo Celular/genética , Línea Celular Tumoral , Proliferación Celular , Femenino , Técnicas de Silenciamiento del Gen , Humanos , Antígeno Nuclear de Célula en Proliferación/metabolismo , Proteínas Proto-Oncogénicas c-bcl-2/metabolismo , Interferencia de ARN , ARN Interferente Pequeño/genética , Células Tumorales Cultivadas , Proteína X Asociada a bcl-2/metabolismo , Proteína de Unión al GTP rhoA/metabolismoRESUMEN
Gemcitabine and doxorubicin were separately chemically linked to biodegradable polymers to prepare polymer-gemcitabine and polymer-doxorubicin conjugates. Moreover, the two conjugates can self-assemble into micelles with both gemcitabine and doxorubicin. In this way, the two anticancer drugs were combined. The in vitro MTT assay with these combined drugs showed synergistic effect compared to single use of each drug.
Asunto(s)
Desoxicitidina/análogos & derivados , Doxorrubicina/química , Doxorrubicina/farmacología , Portadores de Fármacos/química , Micelas , Nanopartículas/química , Antineoplásicos/química , Antineoplásicos/farmacología , Línea Celular Tumoral , Supervivencia Celular/efectos de los fármacos , Desoxicitidina/química , Desoxicitidina/farmacología , Células Hep G2 , Humanos , GemcitabinaRESUMEN
Due to the heterogeneity of lymph node examination and the conflicting results existing for the same classification of lymph node ratio (LNR), it is necessary to conduct a meta-analysis to evaluate the prognostic effects of different LNRs on breast cancer. PubMed, EMBASE, and ISI Web of Knowledge were searched to find all published cohort studies that evaluated the prognostic value of different LNRs on breast cancer. The outcomes were overall survival (OS), disease-free survival (DFS), breast cause-special survival (BCCS), mortality, locoregional recurrence (LRR), and distant metastasis. Data was analyzed using comprehensive meta-analysis software version 2.0, and 23 studies were included. The available evidence showed that LNR was a prognostic predictor for breast cancer, especially for clinically node-positive breast cancer, but the available evidence could not judge which cutoff point is the most reliable. Meanwhile, the cutoff values 0.2 and 0.65 could be suitable to predict breast cancer OS, DFS, BCCS, and mortality.