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The long non‑coding RNA (lncRNA) differentiation antagonizing non‑protein coding RNA (DANCR) has been reported to be a novel potential biomarker for colon cancer prognosis. However, its functional role in colon cancer remains unknown. In the present study, DANCR expression in colon cancer cell lines was determined by reverse transcription‑quantitative polymerase chain reaction. Cell Counting kit‑8 assay, colony formation assay, flow cytometry, Hoechst 33258 staining and western blotting were utilized to investigate the effect and mechanism of DANCR in the regulation of colon cancer growth. Establishment of a xenograft tumor model followed by terminal deoxynucleotidyl transferase (TdT) dUTP nick‑end labeling assay and immunohistochemical staining were performed to confirm the findings in vitro. DANCR was revealed to be overexpressed in all human colon cancer cell lines. Silencing DANCR by small interfering RNA significantly inhibited cell proliferation and colony formation. Flow cytometry analyses and Hoechst 33258 staining revealed that apoptosis was induced upon DANCR‑knockdown. Silencing DANCR was revealed to efficiently impair colon tumor growth by promoting caspase 3 expression and tumor apoptosis. In summary, the results of the present study demonstrated that DANCR is a potential therapeutic target in colon cancer. [ABSTRACT FROM AUTHOR]

Increasing evidence suggests that Fusobacterium nucleatum is involved in colorectal carcinogenesis. Previous studies have explored whether F. nucleatum may trigger colonic epithelial-mesenchymal transition. The results of the present study demonstrated that F. nucleatum enhances the proliferation and invasion of NCM460 cells compared with that of normal control and DH5α cells. Furthermore, F. nucleatum significantly increased the phosphorylation of p65 (a subunit of nuclear factor-κB), as well as the expression of interleukin (IL)-6, IL-1β and matrix metalloproteinase (MMP)-13. Additionally, F. nucleatum infection did not affect the expression levels of epithelial (E-)cadherin and β-catenin. E-cadherin knockdown in NCM460 cells did not induce the activation of inflammatory responses in response to F. nucleatum infection, whereas it increased inflammation in response to β-catenin silencing. F. nucleatum infection could not increase the proportion of cells at S phase when E-cadherin was silenced. Nevertheless, F. nucleatum infection enhanced the proportion of NCM460 cells at S phase when transfected with small interfering RNAs to knock down β-catenin expression. In conclusion, the results of the present study demonstrated that F. nucleatum infection interacted with E-cadherin instead of β-catenin, which in turn enhances the malignant phenotype of colorectal cancer cells. [ABSTRACT FROM AUTHOR]

A major cause of treatment failure in advanced colon cancer is resistance to chemotherapy. p38 mitogen-activated protein kinase (MAPK) has been associated with cellular apoptosis and plays an important role in multidrug resistance (MDR) in cancer cells. In the present study the effect of p38 MAPK on the sensitivity of 5-fluorouracil (5-FU)-resistant SW480 (SW480/5-FU) human colon cancer cells to noscapine was investigated. Following p38 MAPK interference, the inhibitory effect of noscapine on cell viability and proliferation was increased in the SW480/5-FU cells and there was also a decrease in the expression level of minichromosome maintenance proteins, recombinant Ki-67 and proliferating cell nuclear antigen. Inhibition of p38 MAPK also enhanced noscapine-induced G1-phase cell cycle arrest in the SW480/5-FU cells and there was also a decrease in the protein and mRNA expression level of cyclin D, cyclin E and cyclin-dependent kinase 2, and an increase in the expression level of P57. Furthermore, p38 MAPK interference increased noscapine-induced apoptosis of the SW480/5-FU cells and there was an increase in the protein and mRNA expression level of caspases-3 and 8 and Bax, and decreased Bcl-2 expression level. The sensitivity of the SW480/5-FU cells to noscapine was also increased following p38 MAPK interference, as demonstrated by MDR inhibition via decreased Akt activity and reduced protein expression level of the MDR proteins P-glycoprotein, multidrug resistance protein 1 and ATP-binding cassette G2. These observations indicated that inhibition of p38 MAPK increased the sensitivity of the SW480/5-FU cells to noscapine by suppressing proliferation, induction of cell cycle arrest and apoptosis, and reversal of MDR in the SW480/5-FU cells. [ABSTRACT FROM AUTHOR]