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miR-98 targets ITGB3 to inhibit proliferation, migration, and invasion of non-small-cell lung cancer.

Ni R, Huang Y, Wang J - Onco Targets Ther (2015)

Bottom Line: Finally, we transplanted miR-98 expressing A549 cells into nude mice to observe the effect of miR-98 on tumor growth in vivo.Furthermore, we identified that miR-98 exerted inhibitory roles by directly binding to 3'-UTR of ITGB3 mRNA, thus negatively regulated the expression of ITGB3.Interestingly, upon restoring the expression of ITGB3, the effect of miR-98 on cell proliferation was partially reversed.

View Article: PubMed Central - PubMed

Affiliation: Department of Respiration Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, People's Republic of China.

ABSTRACT

Background: Accumulating evidence has emphasized causative links between aberrant microRNA (miR) expression patterns and cancer development. Abnormally expressed miRNA-98 (miR-98) was found in certain types of human cancers. The biological roles of miR-98 in lung cancer, however, remain largely undefined.

Methods: We evaluated the expression of miR-98 in normal lung tissues, lung cancer tissues, normal human bronchial epithelial cells, and lung cancer cells using quantitative real-time polymerase chain reaction. Effect of miR-98 on proliferation of lung cancer cells was investigated using MTT assay and colony formation assay. Transwell assay was used to assess the effects of miR-98 on migration and invasion of lung cancer cells. Whether miR-98 targets the 3'-untranslated region (3'-UTR) of integrin β3 (ITGB3) coding gene ITGB3 mRNA was ascertained using luciferase reporter assay. Finally, we transplanted miR-98 expressing A549 cells into nude mice to observe the effect of miR-98 on tumor growth in vivo.

Results: We confirmed that miR-98 was frequently low expressed in lung cancer tissues and human lung cancer cells. Reintroduction of miR-98 into lung cancer cells inhibited cell proliferation, migration, and invasion in vitro and suppressed tumor formation in a nude mouse model. Furthermore, we identified that miR-98 exerted inhibitory roles by directly binding to 3'-UTR of ITGB3 mRNA, thus negatively regulated the expression of ITGB3. Interestingly, upon restoring the expression of ITGB3, the effect of miR-98 on cell proliferation was partially reversed.

Conclusion: Our findings suggest that miR-98 prevents proliferation, migration, and invasion of lung cancer cells by directly binding to the 3'-UTR of ITGB3 mRNA and could be a promising treatment option in anticancer therapy.

No MeSH data available.


Related in: MedlinePlus

miR-98 suppresses tumor formation in vivo.Notes: (A) miR-98 overexpressing cells or control A549 cells were injected subcutaneously into nude mice (n=6). The tumor volumes were measured every 5 days, and the mice were sacrificed on day 25. miR-98 decreases the tumor volumes. *P<0.05 vs controls. (B) miR-98 reduces tumor weights. (C) The level of ITGB3 is decreased in miR-98 overexpressing A549 cells. **P<0.01 vs controls.
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f4-ott-8-2689: miR-98 suppresses tumor formation in vivo.Notes: (A) miR-98 overexpressing cells or control A549 cells were injected subcutaneously into nude mice (n=6). The tumor volumes were measured every 5 days, and the mice were sacrificed on day 25. miR-98 decreases the tumor volumes. *P<0.05 vs controls. (B) miR-98 reduces tumor weights. (C) The level of ITGB3 is decreased in miR-98 overexpressing A549 cells. **P<0.01 vs controls.

Mentions: The effect of miR-98 on lung tumor was verified in nude mice models. As shown in Figure 4A, compared with those in the control group, the tumors notably shrank in the miR-98 mimics group after 10 days, 15 days, 20 days, and 25 days. The final tumor weight was also reduced in the miR-98 mimics group (Figure 4B), and ITGB3 was a downregulated expression in the xenografts of miR-98 mimics group compared to that in the control group (Figure 4C).


miR-98 targets ITGB3 to inhibit proliferation, migration, and invasion of non-small-cell lung cancer.

Ni R, Huang Y, Wang J - Onco Targets Ther (2015)

miR-98 suppresses tumor formation in vivo.Notes: (A) miR-98 overexpressing cells or control A549 cells were injected subcutaneously into nude mice (n=6). The tumor volumes were measured every 5 days, and the mice were sacrificed on day 25. miR-98 decreases the tumor volumes. *P<0.05 vs controls. (B) miR-98 reduces tumor weights. (C) The level of ITGB3 is decreased in miR-98 overexpressing A549 cells. **P<0.01 vs controls.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4590683&req=5

f4-ott-8-2689: miR-98 suppresses tumor formation in vivo.Notes: (A) miR-98 overexpressing cells or control A549 cells were injected subcutaneously into nude mice (n=6). The tumor volumes were measured every 5 days, and the mice were sacrificed on day 25. miR-98 decreases the tumor volumes. *P<0.05 vs controls. (B) miR-98 reduces tumor weights. (C) The level of ITGB3 is decreased in miR-98 overexpressing A549 cells. **P<0.01 vs controls.
Mentions: The effect of miR-98 on lung tumor was verified in nude mice models. As shown in Figure 4A, compared with those in the control group, the tumors notably shrank in the miR-98 mimics group after 10 days, 15 days, 20 days, and 25 days. The final tumor weight was also reduced in the miR-98 mimics group (Figure 4B), and ITGB3 was a downregulated expression in the xenografts of miR-98 mimics group compared to that in the control group (Figure 4C).

Bottom Line: Finally, we transplanted miR-98 expressing A549 cells into nude mice to observe the effect of miR-98 on tumor growth in vivo.Furthermore, we identified that miR-98 exerted inhibitory roles by directly binding to 3'-UTR of ITGB3 mRNA, thus negatively regulated the expression of ITGB3.Interestingly, upon restoring the expression of ITGB3, the effect of miR-98 on cell proliferation was partially reversed.

View Article: PubMed Central - PubMed

Affiliation: Department of Respiration Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, People's Republic of China.

ABSTRACT

Background: Accumulating evidence has emphasized causative links between aberrant microRNA (miR) expression patterns and cancer development. Abnormally expressed miRNA-98 (miR-98) was found in certain types of human cancers. The biological roles of miR-98 in lung cancer, however, remain largely undefined.

Methods: We evaluated the expression of miR-98 in normal lung tissues, lung cancer tissues, normal human bronchial epithelial cells, and lung cancer cells using quantitative real-time polymerase chain reaction. Effect of miR-98 on proliferation of lung cancer cells was investigated using MTT assay and colony formation assay. Transwell assay was used to assess the effects of miR-98 on migration and invasion of lung cancer cells. Whether miR-98 targets the 3'-untranslated region (3'-UTR) of integrin β3 (ITGB3) coding gene ITGB3 mRNA was ascertained using luciferase reporter assay. Finally, we transplanted miR-98 expressing A549 cells into nude mice to observe the effect of miR-98 on tumor growth in vivo.

Results: We confirmed that miR-98 was frequently low expressed in lung cancer tissues and human lung cancer cells. Reintroduction of miR-98 into lung cancer cells inhibited cell proliferation, migration, and invasion in vitro and suppressed tumor formation in a nude mouse model. Furthermore, we identified that miR-98 exerted inhibitory roles by directly binding to 3'-UTR of ITGB3 mRNA, thus negatively regulated the expression of ITGB3. Interestingly, upon restoring the expression of ITGB3, the effect of miR-98 on cell proliferation was partially reversed.

Conclusion: Our findings suggest that miR-98 prevents proliferation, migration, and invasion of lung cancer cells by directly binding to the 3'-UTR of ITGB3 mRNA and could be a promising treatment option in anticancer therapy.

No MeSH data available.


Related in: MedlinePlus