摘要
Backgroup: Lung cancer is the leading cause of cancer deaths worldwide. Recent studies have demonstrated the function of TRIM28 as an important regulator for carcinogenesis, however, the role of TRIM28 in the development or maintenance of the malignant cell phenotype has not been studied. Objective: To study the biological function of TRIM28 in NSCLC both in vitro and in vivo Methods: The colony formation and MTT assay were done to observed whether TRIM28 siRNAinhibited tumor growth and proliferation in vitro. Analysis of DNA content was performed to determine whether inhibition of TRIM28 affected cell cycle. The stable silencing was established in PAa, and then the cells were subcutaneously injected into BALB/c nu/nu mice. The tumors were measured every two days and the relative tumor volumes were calculated. To detect apoptotic cells, TUNEL assay was used. Results: In soft agar, PAa transfected with control siRNA formed 504 colonies, while those transfected with TRIM28 siRNA formed 215 colonies(P < 0.05). The cell proliferation of PAa-TRIM28 siRNA was strongly suppressed in a timedependent manner in MTT assay, while the growth inhibitory effect by control siRNA was not observed. The cell cycles data indicated that PAa cells had a significant population in G0/G1 fraction following transfection with TRIM28 siRNA compared with control siRNA. The average tumor weight in BALB/c nu/nu mice injected with PAa-TRIM28 siRNA was dramatically lower than in mice injected with PAa-control siRNA, suggesting that the knockdown of TRIM28 is directly involved in inhibiting tumor growth. The extent of apoptosis(number of TUNEL positive cells) was 12.5±1.47 in the TRIM28 siRNA group, while 0.89±0.67 in control group(P < 0.05).Conclusion: Knockdown of TRIM28 inhibited tumor growth and could be a new potential therapeutic target in NSCLC.
Backgroup: Lung cancer is the leading cause of cancer deaths worldwide. Recent studies have demonstrated the function of TRIM28 as an important regulator for carcinogenesis, however, the role of TRIM28 in the development or maintenance of the malignant cell phenotype has not been studied. Objective: To study the biological function of TRIM28 in NSCLC both in vitro and in vivo Methods: The colony formation and MTT assay were done to observed whether TRIM28 siRNAinhibited tumor growth and proliferation in vitro. Analysis of DNA content was performed to determine whether inhibition of TRIM28 affected cell cycle. The stable silencing was established in PAa, and then the cells were subcutaneously injected into BALB/c nu/nu mice. The tumors were measured every two days and the relative tumor volumes were calculated. To detect apoptotic cells, TUNEL assay was used. Results: In soft agar, PAa transfected with control siRNA formed 504 colonies, while those transfected with TRIM28 siRNA formed 215 colonies(P < 0.05). The cell proliferation of PAa-TRIM28 siRNA was strongly suppressed in a timedependent manner in MTT assay, while the growth inhibitory effect by control siRNA was not observed. The cell cycles data indicated that PAa cells had a significant population in G0/G1 fraction following transfection with TRIM28 siRNA compared with control siRNA. The average tumor weight in BALB/c nu/nu mice injected with PAa-TRIM28 siRNA was dramatically lower than in mice injected with PAa-control siRNA, suggesting that the knockdown of TRIM28 is directly involved in inhibiting tumor growth. The extent of apoptosis(number of TUNEL positive cells) was 12.5±1.47 in the TRIM28 siRNA group, while 0.89±0.67 in control group(P < 0.05).Conclusion: Knockdown of TRIM28 inhibited tumor growth and could be a new potential therapeutic target in NSCLC.
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