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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 inhibits migration and invasion of lung cancer cells.Notes: (A and B) The number of migrated PC9 and A549 cells is decreased after transfection with miR-98 mimics. *P<0.05, **P<0.01 vs controls. (C and D) Overexpression of miR-98 reduces the number of invaded PC9 and A549 cells. *P<0.05 vs controls.
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f2-ott-8-2689: miR-98 inhibits migration and invasion of lung cancer cells.Notes: (A and B) The number of migrated PC9 and A549 cells is decreased after transfection with miR-98 mimics. *P<0.05, **P<0.01 vs controls. (C and D) Overexpression of miR-98 reduces the number of invaded PC9 and A549 cells. *P<0.05 vs controls.

Mentions: The effect of miR-98 on cell migration and invasion in PC9 and A549 lung cancer cells was studied by transwell assays. As shown in Figure 2A and B, compared with the control group, the number of migrated cells was only 39.6±7.5 and 30.3±5.8 in PC 9 and A549 cells, respectively, in the miR-98 mimics group, whereas the corresponding cell number was 109.8±10.3 and 87.6±13.9, respectively, in the control group. The number of invaded cells was 16.9±2.1 and 25.8±2.5 in PC9 and A549 cells transfected with miR-98 mimics, compared to the cells transfected with controls, with the invaded cell number of 36.3±4.7 and 52.6±6.3, respectively (Figure 2C and D).


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 inhibits migration and invasion of lung cancer cells.Notes: (A and B) The number of migrated PC9 and A549 cells is decreased after transfection with miR-98 mimics. *P<0.05, **P<0.01 vs controls. (C and D) Overexpression of miR-98 reduces the number of invaded PC9 and A549 cells. *P<0.05 vs controls.
© Copyright Policy
Related In: Results  -  Collection

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

f2-ott-8-2689: miR-98 inhibits migration and invasion of lung cancer cells.Notes: (A and B) The number of migrated PC9 and A549 cells is decreased after transfection with miR-98 mimics. *P<0.05, **P<0.01 vs controls. (C and D) Overexpression of miR-98 reduces the number of invaded PC9 and A549 cells. *P<0.05 vs controls.
Mentions: The effect of miR-98 on cell migration and invasion in PC9 and A549 lung cancer cells was studied by transwell assays. As shown in Figure 2A and B, compared with the control group, the number of migrated cells was only 39.6±7.5 and 30.3±5.8 in PC 9 and A549 cells, respectively, in the miR-98 mimics group, whereas the corresponding cell number was 109.8±10.3 and 87.6±13.9, respectively, in the control group. The number of invaded cells was 16.9±2.1 and 25.8±2.5 in PC9 and A549 cells transfected with miR-98 mimics, compared to the cells transfected with controls, with the invaded cell number of 36.3±4.7 and 52.6±6.3, respectively (Figure 2C and D).

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