Accumulating evidence has proved that long noncoding RNAs (lncRNAs) are involved in cancer progression. The abnormal expression of lncRNAs might mediate cancer in various ways. Liver hepatocellular carcinoma (LIHC) is the third leading cause of tumor‐related deaths. Due to the difficulty in its early recognition, the therapeutic outcomes of LIHC are far from satisfactory. The lncRNA Coagulation Factor XI Antisense RNA 1 (F11‐AS1) is underexpressed in LIHC and suppresses LIHC progression in return. F11‐AS1 can bind with and negatively regulate miR‐3146, while miR‐3146 can bind with and negatively regulate PTEN. Moreover, F11‐AS1 positively regulates the messenger RNA and protein level of PTEN. Also, miR‐3146, F11‐AS1, and PTEN could all be immunoprecipitated by antibody against Ago2, indicating the existence of RNA–induced silencing complex. Therefore, F11‐AS1 mediates PTEN expression by acting as competing endogenous RNA of miR‐3146. Further rescue assays demonstrated that F11‐AS1 suppressed LIHC progression via such pattern. To sum up, F11‐AS1 suppresses LIHC progression by competitively binding with miR‐3146 to regulate PTEN expression. The F11‐AS1/miR‐3146/PTEN axis is brand new. Taken together, the results indicate that F11‐AS1 might serve as a therapeutic target of LIHC.
The homeobox gene, CDX2, plays a major role in development, especially in the gut, and also functions as a tumor suppressor in the adult colon. In the present study, we investigated the effects of CDX2 expression on the proliferation, migration, and apoptosis of the human colon cancer cell line, Lovo. Lovo cells exogenously expressing CDX2 exhibited no significant differences in the percentage of cells in G1- and S-phase or in apoptosis, as determined by flow cytometry. MTT assay also confirmed that CDX2 expression had no effect on proliferation in these cells. Interestingly, conditioned medium collected from CDX2-overexpressing Lovo cells showed a significant decrease in secretion of MMP-2 and the invasive potential of these cells was significantly inhibited. Collectively, these data suggest that CDX2 may play a critical role in the migration and metastasis of colon carcinoma and over-expression of CDX2 in colon cancer cells markedly inhibits invasion. Based on these results, exogenous expression of CDX2 might be a promising option in the treatment of colon carcinoma.
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