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Si-RNA mediated knockdown of CELF1 gene suppressed the proliferation of human lung cancer cells.

Wu LN, Xue YJ, Zhang LJ, Ma XM, Chen JF - Cancer Cell Int. (2013)

Bottom Line: Lentiviral-mediated transfection of CELF1 siRNA effectively silenced the expression of CELF1 in both A549 and H1299 cells.Colony formation assays revealed a reduction in the number and size of lung cancer cell colonies from CELF1 knockdown.These results indicated that CELF1 may have significant roles in the progression of lung cancer, and suggested that siRNA mediated silencing of CELF1 could be an effective tool in lung cancer treatment.

View Article: PubMed Central - HTML - PubMed

Affiliation: Key laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Thoracic Surgery II, Peking University Cancer Hospital & Institute, Beijing 100142, China. chengjinfeng123@163.com.

ABSTRACT

Background: Lung cancer is the leading cause of cancer-related death in the world, with metastasis as the main reason for the mortality. CELF1 is an RNA-binding protein controlling the post-transcriptional regulation of genes related to cell survival. As yet, there is little knowledge of CELF1 expression and biological function in lung cancer. This study investigated the expression levels of CELF1 in lung cancer tissues and the biological function of CELF1 in lung cancer cells.

Methods: CELF1 mRNA expression was determined in lung cancer and normal tissues, and the relationship between the expression level of CELF1 and clinicopathological parameters was evaluated. The biological function of CELF1 in A549 and H1299 lung cancer cell lines growth was examined.

Results: The expression of CELF1 was higher in human lung cancer tissues compared with the normal lung tissue. Lentiviral-mediated transfection of CELF1 siRNA effectively silenced the expression of CELF1 in both A549 and H1299 cells. Moreover, CELF1 knockdown markedly reduced the survival rate of lung cancer cells. Colony formation assays revealed a reduction in the number and size of lung cancer cell colonies from CELF1 knockdown.

Conclusion: These results indicated that CELF1 may have significant roles in the progression of lung cancer, and suggested that siRNA mediated silencing of CELF1 could be an effective tool in lung cancer treatment.

No MeSH data available.


Related in: MedlinePlus

Effect of CELF1 gene knockdown on the colony forming ability of lung cancer cells. (A, B) The cancer cell colonies under light, bright field and fluorescence microscopy. The colonies were stained with Giemsa staining. The images show comparison of the size of colonies in normal, CELF1-silenced and non-silenced lung cancer cells. (C, D) The number of colonies in normal, CELF1-silenced and non-silenced lung cancer cells. The values represents the mean from three independent experiments; bars represent SD. **P < 0.01, ***P < 0.001 compared with controls.
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Figure 5: Effect of CELF1 gene knockdown on the colony forming ability of lung cancer cells. (A, B) The cancer cell colonies under light, bright field and fluorescence microscopy. The colonies were stained with Giemsa staining. The images show comparison of the size of colonies in normal, CELF1-silenced and non-silenced lung cancer cells. (C, D) The number of colonies in normal, CELF1-silenced and non-silenced lung cancer cells. The values represents the mean from three independent experiments; bars represent SD. **P < 0.01, ***P < 0.001 compared with controls.

Mentions: Lung cancer cells tend to form large cell colonies while in culture; therefore, we next evaluated the effect of CELF1 silencing on the colony forming ability of lung cancer cells. As shown in Figure 5A and B, the size of colonies in CELF1-silenced A549 and H1299 cells was markedly reduced compared with the control groups. Similarly, the number of colonies was also significantly (P < 0.001) reduced with the CELF1 gene knockdown. Together these results indicate that CELF1 plays an important role in the growth progression of lung cancer cells.


Si-RNA mediated knockdown of CELF1 gene suppressed the proliferation of human lung cancer cells.

Wu LN, Xue YJ, Zhang LJ, Ma XM, Chen JF - Cancer Cell Int. (2013)

Effect of CELF1 gene knockdown on the colony forming ability of lung cancer cells. (A, B) The cancer cell colonies under light, bright field and fluorescence microscopy. The colonies were stained with Giemsa staining. The images show comparison of the size of colonies in normal, CELF1-silenced and non-silenced lung cancer cells. (C, D) The number of colonies in normal, CELF1-silenced and non-silenced lung cancer cells. The values represents the mean from three independent experiments; bars represent SD. **P < 0.01, ***P < 0.001 compared with controls.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3842801&req=5

Figure 5: Effect of CELF1 gene knockdown on the colony forming ability of lung cancer cells. (A, B) The cancer cell colonies under light, bright field and fluorescence microscopy. The colonies were stained with Giemsa staining. The images show comparison of the size of colonies in normal, CELF1-silenced and non-silenced lung cancer cells. (C, D) The number of colonies in normal, CELF1-silenced and non-silenced lung cancer cells. The values represents the mean from three independent experiments; bars represent SD. **P < 0.01, ***P < 0.001 compared with controls.
Mentions: Lung cancer cells tend to form large cell colonies while in culture; therefore, we next evaluated the effect of CELF1 silencing on the colony forming ability of lung cancer cells. As shown in Figure 5A and B, the size of colonies in CELF1-silenced A549 and H1299 cells was markedly reduced compared with the control groups. Similarly, the number of colonies was also significantly (P < 0.001) reduced with the CELF1 gene knockdown. Together these results indicate that CELF1 plays an important role in the growth progression of lung cancer cells.

Bottom Line: Lentiviral-mediated transfection of CELF1 siRNA effectively silenced the expression of CELF1 in both A549 and H1299 cells.Colony formation assays revealed a reduction in the number and size of lung cancer cell colonies from CELF1 knockdown.These results indicated that CELF1 may have significant roles in the progression of lung cancer, and suggested that siRNA mediated silencing of CELF1 could be an effective tool in lung cancer treatment.

View Article: PubMed Central - HTML - PubMed

Affiliation: Key laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Thoracic Surgery II, Peking University Cancer Hospital & Institute, Beijing 100142, China. chengjinfeng123@163.com.

ABSTRACT

Background: Lung cancer is the leading cause of cancer-related death in the world, with metastasis as the main reason for the mortality. CELF1 is an RNA-binding protein controlling the post-transcriptional regulation of genes related to cell survival. As yet, there is little knowledge of CELF1 expression and biological function in lung cancer. This study investigated the expression levels of CELF1 in lung cancer tissues and the biological function of CELF1 in lung cancer cells.

Methods: CELF1 mRNA expression was determined in lung cancer and normal tissues, and the relationship between the expression level of CELF1 and clinicopathological parameters was evaluated. The biological function of CELF1 in A549 and H1299 lung cancer cell lines growth was examined.

Results: The expression of CELF1 was higher in human lung cancer tissues compared with the normal lung tissue. Lentiviral-mediated transfection of CELF1 siRNA effectively silenced the expression of CELF1 in both A549 and H1299 cells. Moreover, CELF1 knockdown markedly reduced the survival rate of lung cancer cells. Colony formation assays revealed a reduction in the number and size of lung cancer cell colonies from CELF1 knockdown.

Conclusion: These results indicated that CELF1 may have significant roles in the progression of lung cancer, and suggested that siRNA mediated silencing of CELF1 could be an effective tool in lung cancer treatment.

No MeSH data available.


Related in: MedlinePlus