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首页> 外文期刊>Combinatorial chemistry & high throughput screening >Effects of Long Noncoding RNA AK093407 on the Biological Behavior of Colon Cancer Cells and the Underlying Mechanism
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Effects of Long Noncoding RNA AK093407 on the Biological Behavior of Colon Cancer Cells and the Underlying Mechanism

机译：Effects of Long Noncoding RNA AK093407 on the Biological Behavior of Colon Cancer Cells and the Underlying Mechanism

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Introduction: The incidence of colorectal cancer is steadily increasing, and the detection of related molecular targets is critical for its diagnosis and treatment. Long noncoding RNA (lncRNA) can play a regulatory role before and after genome transcription, and epigenetic regulation is involved in the process of tumorigenesis and tumor development. Methods: In this study, qRT-PCR was performed to evaluate the expression of AK093407 in colon cancer and colon para-carcinoma tissues and HCT-15 and HCT-116 cells. SiRNA was transfected into HCT-15 and HCT-116 cells to knock down lncRNA-AK093407. Then, MTT assay was used to test cell proliferation, and flow cytometry was used to test apoptosis and cell cycle. The protein expression of caspase-3, caspase-8, caspase-9, bax, bcl-2, cyclin-A1, cyclin-B1, cyclin-D1, cyclin-E1, p21, p27, and p-Stat3 was determined by Western blot. Results: The results showed that the expression of AK093407 in human colon cancer tissue was higher than in para-carcinoma tissue. The amount of AK093407 in HCT-15 and HCT-116 cells was higher than that in normal colorectal epithelial NM460 cells. When AK093407 was silenced, the proliferation of HCT-15 and HCT-116 cells decreased, the apoptosis rate increased, the cell cycle was arrested in the G1/S phase, the expression of caspase-3, caspase-8, caspase-9, bax, cyclin-A1, cyclin-B1, p21, p27 increased, and the expression of bcl-2, cyclin-D1, cyclin-E1, p-Stat3 decreased. Conclusion: These results showed that knockdown of AK093407 could inhibit colon cancer cell proliferation, induce apoptosis and cell cycle arrest, influence the expression of vital factors in mitochondrial apoptosis pathway and cell cycle regulatory pathway, and may negatively regulate JAK/STAT3 through down-regulating p-Stat3.

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