Exosomes derived from LS174T and LSC human colon cancer cell lines were isolated from cell culture supernatant and pulled down using tetraspanin-specific antibody CD63 immunoaffinity magnetic beads.
Predictors of reoperation were TNM IV (OR 5.06), surgical complications within 30 days (OR 1.98), and type and site of tumor (OR 1.72) in colon cancer and being male (OR 1.52), age (OR 1.80), stoma (OR 1.87), and surgical complications within 1 month (OR 1.95) in rectal cancer.
To explore the effects and mechanisms of BMP1 on the EMT of colon cancer, a BMP1 overexpression plasmid vector was used to interfere with SW620 cells and real-time fluorescence quantitative RNA and western blotting were used to detect the effects of BMP1 on the transcription and translation of COL1A1 and COL1A2 genes, as well as EMT-related genes, including beta-catenin, vimentin, and E-cadherin (E-Cad) genes in SW620 cells.
The K-R and K-Q mutants were constructed and the impacts of KDM2B on demethylation of nucleosomal substrates, p21, and puma transcription and the carcinogenesis of colon cancer were probed.
In the present study, SW620, a colon cancer cell line that stably expresses CDR1‑AS RNA circularized, was established using the laccase 2 gene cassette, and its biological function associated with malignant behavior was determined.
Our findings suggest that elevated ATP5E expression could serve as a marker of distant metastasis and a poor prognosis in colon cancer, and ATP5E functions via modulating AMPK-AKT-HIF1α signaling.
USP47 deficiency impairs transcriptional activity of SATB1 target genes and inhibits colon cancer cell proliferation, migration, and tumorigenesis in a mouse model of colon cancer.
Knockdown of PYROXD1 arrested the cell cycle, and induced late apoptosis in colon cancer cell line HCT116 DISCUSSION: Taken together, these results revealed the critical roles of PYROXD1 in regulating cell cycle and apoptosis and possibly will signify its therapeutic potential for targeting colorectal cancer models.
CKS1 is highly expressed in colon cancer tissues, and the overexpression of CKS1 promotes cell proliferation and colony formation in both HCT116 (originating from primary colon cancer) and SW620 (originating from metastatic tumor nodules of colon cancer) cells.
Collectively, ATG3 upregulation, caused by downregulated miR-435-5p, promotes proliferation and invasion via an autophagy-dependent manner in colon cancer suggesting that miR-431-5p/ATG3/autophagy may be a potential therapeutic target in colon cancer.
Depletion of SSBP1 in colon cancer cell lines was able to trigger loss of mitochondrial mass and an increase in tumor cell death, and this effect that was further accentuated in the presence of the common chemotherapy drug cisplatin.
We have already demonstrated <i>in vitro</i> that LOX-1 expression correlates to the aggressiveness of human colon cancer and its downregulation weakens the tumoral phenotype, indicating its potential function as a biomarker and a target in CRC therapy.
To study the effect of RITA (MDM2-p53 interaction inhibitor) and its action along with genotoxic drug cisplatin was evaluated on COLO-205 colon cancer and PC-3 prostate cancer cells.
The results of the present study support a mechanism of underlying oncogenic activities by means of Ebp1 through regulation of TIF-90-mediated rRNA synthesis and suggest the potential therapeutic treatment of colon cancer by targeting Ebp1 and its signaling.
In conclusion, our data provided evidence for the regulatory network of UCA1/miR-28-5p/HOXB3 in colon cancer, suggesting that UCA1, miR-28-5p, and HOXB3 are the potential targets for colon cancer therapy.