Abstract
To investigate the expression of long non-coding RNA (lncRNA) DMTF1v4 in colon cancer, and the relationship between its expression and disease occurrence. Human colon cancer tissues and para-carcinoma tissues were harvested. The expression of lncRNA DMTF1v4 was measured by semi-quantitative PCR. The expression of DMTF1v4 in HT-29 colon cancer cells was downregulated using siRNA, and the effect of its downregulation on cell growth was determined by MTT assay and plate clone assay. The effect of DMTF1v4 downregulation on colon cancer cell migration was determined using a transwell assay and scratch wound assay. The effect of DMTF1v4 on colon cancer cell apoptosis was determined using Annexin V/PI double-staining. The changes in p-ERK, p-JNK, and p-p38 were measured by Western blot. HT-29 cells with downregulated DMTF1v4 expression were used to establish the subcutaneous heterotopic transplantation tumor model in nude mice to study the effect of DMTF1v4 on tumor growth in animals. Compared with para-carcinoma tissue, lncRNA DMTF1v4 in colon cancer tissue was highly expressed (p<0.001). Downregulating lncRNA DMTF1v4 in HT-29 cells showed that lncRNA DMTF1v4 promotes cell proliferation and migration, and suppresses apoptosis (p<0.05). The effect of lncRNA DMTF1v4 on the ERK/MAPK signaling pathway was evaluated. The expression of p-ERK, p-JNK, and p-p38 was increased significantly compared with the control group (p<0.01). The effect of downregulating DMTF1v4 on tumor growth in animals showed that tumor growth in nude mice was decreased, and the expression of apoptosis-related proteins was increased (p<0.01). The expression of lncRNA DMTF1v4 is elevated in colon cancer tissues; lncRNA DMTF1v4 promotes colon cancer cell proliferation and migration, and inhibits apoptosis by downregulating the expression of p-ERK, p-JNK, and p-p38, thus affecting the progression of colon cancer. This will provide a basis for the development of new clinical treatments for colon cancer.
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