MicroRNAs (miRNAs) can function as tumor suppressor or oncogenic genes. The putative targets of miR-223 include tumor suppressor gene, RhoB. Here we sought to investigate the role of miR-223-RhoB signaling pathway in proliferation of colon cancer. We used Western blot, immunofluorescence staining, or RT-PCR to detect expression levels of miR-223 and RhoB in colon adenocarcinoma and adjacent non-cancerous tissue samples, or in human colon adenocarcinoma cell lines. MTT assay was used to determine proliferation and apoptosis in cell lines. We further used Western blot to determine levels of cell cycle regulators CDK1 and Cyclin B1 with anti-miR-223 or apoptosis with overexpression of RhoB. The expression level of miR-223 was significantly upregulated in clinical samples and cell lines of colon adenocarcinoma, in contrast to down-regulation of RhoB. In addition, we showed that inhibition of miR-223 led to upregulation of RhoB and in turn suppression of proliferation of colon adenocarcinoma. Moreover, inhibition of miR-223 or overexpression of RhoB induced cell arrest or apoptosis in colon adenocarcinoma. These results suggest that miR-223-RhoB signaling pathway plays an important role in modulation of proliferation, cell arrest, and apoptosis in colon cancer.
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http://dx.doi.org/10.1016/j.cbi.2018.04.016 | DOI Listing |
Colon cancer poses a significant threat to global health, and studies have shown a correlation between physical activity (PA) and the incidence of colon cancer. However, existing research has not quantitatively analyzed PA to evaluate its impact on the risk of colon cancer comprehensively. Data related to the study were obtained from the NHANES database for participants aged 20 and above between 2007 and 2018.
View Article and Find Full Text PDFInt J Colorectal Dis
January 2025
Hereditary Digestive Tract Tumors Unit, Fondazione IRCCS Istituto Nazionale Dei Tumori, Via Giacomo Venezian 1, 20133, Milan, Italy.
Purpose: In this study, we investigated the progression of high-grade dysplasia (HGD)/CRC in patients with hereditary colorectal cancer syndromes (HCSS) and concomitant inflammatory bowel diseases (IBDs).
Methods: We described the natural history of a series of patients with confirmed diagnosis of hereditary colorectal cancer syndromes (HCCSs) and concomitant IBDs who were referred to the Hereditary Digestive Tumors Registry at the Fondazione IRCCS Istituto Nazionale dei Tumori of Milan.
Results: Between January 1989 and April 2024, among 450 patients with APC-associated polyposis and 1050 patients with Lynch syndrome (LS), we identified six patients with IBDs (five with UC, one with ileal penetrating CD) and concomitant HCCSs (five with LS, one with APC-associated polyposis).
Sci Rep
January 2025
Ministry of Higher Education, Mataria Technical College, Cairo, 11718, Egypt.
The current work introduces the hybrid ensemble framework for the detection and segmentation of colorectal cancer. This framework will incorporate both supervised classification and unsupervised clustering methods to present more understandable and accurate diagnostic results. The method entails several steps with CNN models: ADa-22 and AD-22, transformer networks, and an SVM classifier, all inbuilt.
View Article and Find Full Text PDFPharmaceutics
December 2024
Department of Pharmaceutical Technology, Faculty of Natural Sciences I, Institute of Pharmacy, Martin Luther University Halle-Wittenberg, Kurt-Mothes-Str. 3, 06120 Halle/Saale, Germany.
Background/objectives: Bringing small interfering RNA (siRNA) into the cell cytosol to achieve specific gene silencing is an attractive but also very challenging option for improved therapies. The first step for successful siRNA delivery is the complexation with a permanent cationic or ionizable compound. This protects the negatively charged siRNA and enables transfection through the cell membrane.
View Article and Find Full Text PDFMolecules
January 2025
Department of Experimental Medicine, Sapienza University of Rome, 00161 Rome, Italy.
Epigenetic abnormalities play a critical role in colon carcinogenesis, making them a promising target for therapeutic interventions. In this study, we demonstrated that curcumin reduces colon cancer cell survival and that a decrease in lysine methylation was involved in such an effect. This correlated with the downregulation of methyltransferases EZH2, MLL1, and G9a, in both wild-type p53 (wtp53) HCT116 cells and mutant p53 (mutp53) SW480 cells, as well as SET7/9 specifically in wtp53 HCT116 cells.
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