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Background Our study aims to investigate the effect of colon cancer-associated transcript-1 (CCAT-1) on colon cancer cells' activity and metabolism under different glucose environments in vitro and in vivo. Methods The levels of proliferation, migration, glucose, lactic acid, glucose metabolism-related enzymes, apoptosis genes, epithelial-mesenchymal transition (EMT) marker proteins, and PI3K/Akt/C-MYC pathway in CCAT-1-silenced SW620 cells cultured with different glucose levels were tested. Twenty BALB/C nude mice with hyperglycemia or normal blood sugar were transplanted with CCAT-1-silenced SW620 cells, blood glucose levels, lactic acid, insulin, and volume of transplanted tumor cells, the expression of EMT marker proteins, and PI3K/Akt/C-MYC pathway was detected. Results The levels of proliferation, migration, glucose, lactic acid, LDH-A, PKM2, and HK2 decreased, apoptosis increased in SW620 cells cultured with low glucose or silenced CCAT-1 (P

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Background Epidemiological studies have found that hyperglycemia, is an independent risk factor for colorectal cancer (CRC), increasing colon cancer incidence and affecting the recurrence, metastasis, and prognosis in colon cancer patients. However, the intercorrelation between hyperglycemia and CRC risk is still unknown, In the present study, we sought to determine whether gene markers, which act in CRC with hyperglycemia, are silenced in CRC without hyperglycemia. Methods In order to characterize the mechanism of functional genes associated with CRC with hyperglycemia, A total 24 CRC and matched controls were sequenced. Through bioinformatics analysis includes differential expression analysis, functional enrichment, new isoform prediction and alternative splicing event identification to found biomarker genes related to CRC development. Results CRC patients with hyperglycemia were compared with patients without hyperglycemia, and we found that 21 genes were upregulated and 27 were downregulated. Further study showed that these genes are possibly of key genes involved in CRC development with hyperglycemia, such as mannan-binding lectin-associated serine protease 3 (MASP3), which has an immunological role in the activation of the complement system. Based on our comprehensive analysis, a cis-regulatory network for hyperglycemic CRC was reconstructed. Conclusions Protein-protein interactions revealed the mechanisms of molecules involved in the interaction of hyperglycemia and cancer development. Our results provide further information on the metabolic pathway interaction with cancer pathways and elucidated the mechanisms of hyperglycemic factors function in cancer development from a transcriptomic perspective.

Introduction The aim of the study was to investigate the effect of CNRIP1 promoter methylation on the proliferative, invasive and migration potential of colorectal cancer cells, including its potential use for the early detection and prognostic assessment of colorectal cancer. Material and methods Quantitative methylation-specific PCR (qMSP) was used to detect the methylation status of the CNRIP1 promoter region in peripheral blood samples drawn from patients with colorectal adenocarcinoma, benign colorectal adenoma, and matched healthy controls. Putative CpG methylation sites were then pyrosequenced. We subsequently suppressed CNRIP1 methylation within colon cancer cells via treatment with 5-azacytidine and overexpressed colon cancer cells by transfection with a CNRIP1-overexpression pcDNA3.0 plasmid. Thereafter, the CNRIP1 methylation status and mRNA and protein expressions levels were determined. Finally, the proliferative, invasive and migration abilities of cell lines were determined with the CCK-8 and Transwell cell assays. Results There were differences in the methylation status at loci 2216, 2226, 2231, 2245, and 2254 within the promoter region of CNRIP1 between patients with colorectal adenocarcinoma, colorectal adenoma, and healthy volunteers. The methylation status of CpG sequence 2245 significantly correlated with tumor diameter, invasion depth, TNM stage, grade, and lymph node metastasis (p < 0.05). The proliferative, invasive and migration abilities of colon cancer cells treated with 5-azaC or transfected with a CNRIP1-overexpression plasmid were significantly impaired relative to negative controls (p < 0.05). Conclusions The methylation status at locus 2245 within the CNRIP1 promoter region has potential value for the early detection and prognostic evaluation of colorectal cancers. Demethylation of the CNRIP1 promoter or overexpression of CNRIP1 can reduce the proliferative and migration abilities of colon cancer cells.

Chicken ovalbumin upstream promoter transcription factor II (COUP-TFII) promotes progression of a variety of tumors. The study was designed to explore the role of COUP-TFII in colorectal carcinoma (CRC) resistance to doxorubicin. The sensitivity of CRC cell lines to doxorubicin was calculated by different proliferation rate measured with cell count kit-8 and EdU (5-Ethynyl-2'-deoxyuridine) assay. The expression of COUP-TFII, Vimentin and E-cadherin were verified using western blot. After doxorubicin administration, CRC cell lines presented apparently down-regulated COUP-TFII, E-cadherin expression and increased Vimentin expression. Besides, COUP-TFII knock-down resulted in significantly increased sensitivity to doxorubicin in all of CRC cell lines, but Twist knock-down presented totally reversed this effect. Furthermore, COUP-TFII knock-down promoted mesenchymal-epithelial transition (MET) in CRC cell lines. After doxorubicin treatment, immediately decreased COUP-TFII expression significantly suppresses CRC cells survival outcomes by suppressing EMT [corrected].

Background: Protein arginine methyltransferases 1 (PRMT1) is over-expressed in a variety of cancers, including lung cancer, and is correlated with a poor prognosis of tumor development. This study aimed to investigate the role of PRMT1 in nonsmall cell lung cancer (NSCLC) migration in vitro . Methods: In this study, PRMT1 expression in the NSCLC cell line A549 was silenced using lentiviral vector-mediated short hairpin RNAs. Cell migration was measured using both scratch wound healing and transwell cell migration assays. The mRNA expression levels of matrix metalloproteinase 2 (MMP-2) and tissue inhibitor of metalloproteinase 1, 2 (TIMP1, 2) were measured using quantitative real-time reverse transcription-polymerase chain reaction. The expression levels of protein markers for epithelial-mesenchymal transition (EMT) (E-cadherin, N-cadherin), focal adhesion kinase (FAK), Src, AKT, and their corresponding phosphorylated states were detected by Western blot. Results: Cell migration was significantly inhibited in the PRMT1 silenced group compared to the control group. The mRNA expression of MMP-2 decreased while TIMP1 and TIMP2 increased significantly. E-cadherin mRNA expression also increased while N-cadherin decreased. Only phosphorylated Src levels decreased in the silenced group while FAK or AKT remained unchanged. Conclusions: PRMT1-small hairpin RNA inhibits the migration abilities of NSCLC A549 cells by inhibiting EMT, extracellular matrix degradation, and Src phosphorylation in vitro .