After the publication of the article, an interested reader drew to the authors' attention that the Du145 'Control' migration panel in Fig. 2C appeared to overlap with the Du145 'Control' invasion panel in Fig. 5A; furthermore, two of the Du145 panels in Fig. 5A also appeared to overlap. The authors have consulted their original data, and realize that these figures were inadvertently assembled incorrectly. The corrected versions of Figs. 2 and 5, incorporating the correct data for the Du145 'Control' panel in Fig. 2C, and the TQ‑/TGF‑β OE‑ invasion and migration panels, and the TQ+/TGF‑β OE+ migration panel, in Fig. 5A, are shown on the next page. These further corrections do not grossly affect the results or the conclusions reported in this work. The authors all agree to this Corrigendum, and are grateful to the Editor of for granting them the opportunity to correct the errors that were made during the assembly of these figures. Lastly, the authors apologize to the readership for any inconvenience these errors may have caused. [Oncology Reports 38: 3592‑3598, 2017; DOI: 10.3892/or.2017.6012].
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http://dx.doi.org/10.3892/or.2023.8491 | DOI Listing |
Biochem Res Int
January 2025
Department of Medical Biochemistry, Faculty of Medicine, Ege University, İzmir, Türkiye.
Recently, it has been shown that protein phosphatase 2A (PP2A) dysfunction was common in many cancer types and was mediated by various inactivation mechanisms. Although many research studies observed antitumor effect of propolis extracts in various types of cancer, the mechanism of effect are still obscure. In this study, we investigated the effect of propolis on PPP2R1A expression and its relationship with apoptosis in the SW-620 (colorectal cancer), DU-145 and PC-3 (prostate cancer), and MCF-7 (breast cancer) cell lines, with WI-38 (healthy fibroblast) cells serving as the control.
View Article and Find Full Text PDFJ Steroid Biochem Mol Biol
January 2025
Laboratory of Experimental Endocrinology, Department of Pharmacology, Escola Paulista de Medicina (EPM), Universidade Federal de São Paulo (UNIFESP), São Paulo, SP 04039-032, Brazil. Electronic address:
The aims of this study were to investigate the localization of non-phosphorylated β‑catenin and Galectin-3 (GAL-3), the regulation of the expression of both proteins by activation of estrogen receptors (ERs) and their role in tumorigenic characteristics of androgen-independent prostate cancer DU-145 cells. DU-145 cells were cultured in the absence (control), and presence of 17β-estradiol (E2). Cells were also untreated or pre-treated with the inhibitor of GAL‑3, VA03, or with a compound that disrupts the complex β-catenin-TCF/LEF transcription factor, PKF 118-310.
View Article and Find Full Text PDFAm J Transl Res
December 2024
Laboratory of Translational Oncology and Experimental Cancer Therapeutics, The Warren Alpert Medical School, Brown University Providence, RI 02903, USA.
Objectives: Prostate cancer (PCa) is a leading cause of cancer death in men worldwide. Approximately 30% of castrate-resistant PCa becomes refractory to therapy due to neuroendocrine differentiation (NED) that is present in <1% of de-novo tumors. First-in-class imipridone ONC201/TIC10 therapy has shown clinical activity against midline gliomas, neuroendocrine tumors, and PCa.
View Article and Find Full Text PDFAsian Pac J Cancer Prev
December 2024
Department of Molecular Biology, EW Villa Medica, Dhaka, Bangladesh.
Objective: This study investigated the potential anticancer properties of Myo-inositol on the DU-145 prostate cancer cell line.
Methods: The DU-145 cells have been treated to different doses of Myo-inositol in order to ascertain the half-maximal inhibitory concentration (IC50) using the trypan blue exclusion assay. The impact of Myo-inositol on proteomic profiles was evaluated using 2D gel electrophoresis and liquid chromatography-mass spectrometry (LC-MS).
Naunyn Schmiedebergs Arch Pharmacol
December 2024
Department of Urology, Tangdu Hospital, Fourth Military Medical University, No.569 Xinsi Road, Xi'an, 710038, Shaanxi, China.
Radiosensitivity is critical for clinical outcomes and overall survival of prostate cancer patients treated with irradiation. Ribociclib and NU7026 have been reported as radiosensitizers in cancer cells, but which are inadequately understood in prostate cancer cells. The present study was performed to investigate the effects of ribociclib, NU7026, and their combination on the radiosensitivity of prostate cancer cells.
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