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Targeted Silencing of S100A8 Gene by miR-24 to Increase Chemotherapy Sensitivity of Endometrial Carcinoma Cells to Paclitaxel.

Lang B, Shang C, Meng L - Med. Sci. Monit. (2016)

Bottom Line: RESULTS The low expression of miR-24 in EC tissues compared with normal control tissues suggests miR-24 might play a role in tumorigenesis of EC.EC HEC-1A cells were transfected with miR-24 agonist (agomiR-24) to up-regulate the expression of miR-24.We used several types of bioinformatic software to predict that miR-24 could specifically combine with the 3' untranslated region (3'UTR) of the S100A8 gene, and this prediction was verified by Western blot and luciferase activities assay.

View Article: PubMed Central - PubMed

Affiliation: School of Health Sciences, Macao Polytechnic Institute, Macao, China (mainland).

ABSTRACT
BACKGROUND The objective of this study was to determine whether miR-24 can regulate malignant proliferation and chemotherapy sensitivity of EC cells by targeted silencing of the S100 Calcium Binding Protein A8 (S100A8) gene. MATERIAL AND METHODS The expression of miR-24 in EC tissues was detected by quantitative real-time PCR. The proliferation ability and chemotherapy sensitivity were analyzed by MTT assay. Bioinformatics software was used to predict some potential target genes of miR-24. Luciferase activity assay was used to verify the relationship between target genes and miR-24. S100A8 protein expression was detected by Western blot analysis. RESULTS The low expression of miR-24 in EC tissues compared with normal control tissues suggests miR-24 might play a role in tumorigenesis of EC. EC HEC-1A cells were transfected with miR-24 agonist (agomiR-24) to up-regulate the expression of miR-24. Up-regulation of miR-24 inhibited the cell proliferation and advanced the chemotherapy sensitivity to paclitaxel in HEC-1A cells significantly. We used several types of bioinformatic software to predict that miR-24 could specifically combine with the 3' untranslated region (3'UTR) of the S100A8 gene, and this prediction was verified by Western blot and luciferase activities assay. The regulation effects of miR-24 enhancement on cell proliferation and chemotherapy sensitivity were largely reversed by S100A8 up-regulation. CONCLUSIONS miR-24 acts as a tumor-suppressing gene to inhibit malignant proliferation and advance chemotherapy sensitivity to paclitaxel in EC by targeted silencing of the S100A8 gene.

No MeSH data available.


Related in: MedlinePlus

(A) Agomir-24 transfection up-regulated the expression of miR-24 in HEC-1A cells (n=5). (B) The cell viability of HEC-1A cells was inhibited by miR-24 enhancement (n=5). (C) Up-regulation of miR-24 decreased the IC50 of paclitaxel in HEC-1A cells (n=5). * P<0.05.
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f2-medscimonit-22-1953: (A) Agomir-24 transfection up-regulated the expression of miR-24 in HEC-1A cells (n=5). (B) The cell viability of HEC-1A cells was inhibited by miR-24 enhancement (n=5). (C) Up-regulation of miR-24 decreased the IC50 of paclitaxel in HEC-1A cells (n=5). * P<0.05.

Mentions: The influences of miR-24 on cell proliferation and chemotherapy sensitivity in HEC-1A cells were investigated. Agomir-24 was transfected into HEC-1A cells to up-regulate miR-24′s expression (Figure 2A). Compare with control cells, the cell proliferation was markedly inhibited by miR-24 enhancement (Figure 2B). Therefore, miR-24 acted as a tumor-suppressing gene in EC cells and suppressed malignant growth of EC cells.


Targeted Silencing of S100A8 Gene by miR-24 to Increase Chemotherapy Sensitivity of Endometrial Carcinoma Cells to Paclitaxel.

Lang B, Shang C, Meng L - Med. Sci. Monit. (2016)

(A) Agomir-24 transfection up-regulated the expression of miR-24 in HEC-1A cells (n=5). (B) The cell viability of HEC-1A cells was inhibited by miR-24 enhancement (n=5). (C) Up-regulation of miR-24 decreased the IC50 of paclitaxel in HEC-1A cells (n=5). * P<0.05.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4920097&req=5

f2-medscimonit-22-1953: (A) Agomir-24 transfection up-regulated the expression of miR-24 in HEC-1A cells (n=5). (B) The cell viability of HEC-1A cells was inhibited by miR-24 enhancement (n=5). (C) Up-regulation of miR-24 decreased the IC50 of paclitaxel in HEC-1A cells (n=5). * P<0.05.
Mentions: The influences of miR-24 on cell proliferation and chemotherapy sensitivity in HEC-1A cells were investigated. Agomir-24 was transfected into HEC-1A cells to up-regulate miR-24′s expression (Figure 2A). Compare with control cells, the cell proliferation was markedly inhibited by miR-24 enhancement (Figure 2B). Therefore, miR-24 acted as a tumor-suppressing gene in EC cells and suppressed malignant growth of EC cells.

Bottom Line: RESULTS The low expression of miR-24 in EC tissues compared with normal control tissues suggests miR-24 might play a role in tumorigenesis of EC.EC HEC-1A cells were transfected with miR-24 agonist (agomiR-24) to up-regulate the expression of miR-24.We used several types of bioinformatic software to predict that miR-24 could specifically combine with the 3' untranslated region (3'UTR) of the S100A8 gene, and this prediction was verified by Western blot and luciferase activities assay.

View Article: PubMed Central - PubMed

Affiliation: School of Health Sciences, Macao Polytechnic Institute, Macao, China (mainland).

ABSTRACT
BACKGROUND The objective of this study was to determine whether miR-24 can regulate malignant proliferation and chemotherapy sensitivity of EC cells by targeted silencing of the S100 Calcium Binding Protein A8 (S100A8) gene. MATERIAL AND METHODS The expression of miR-24 in EC tissues was detected by quantitative real-time PCR. The proliferation ability and chemotherapy sensitivity were analyzed by MTT assay. Bioinformatics software was used to predict some potential target genes of miR-24. Luciferase activity assay was used to verify the relationship between target genes and miR-24. S100A8 protein expression was detected by Western blot analysis. RESULTS The low expression of miR-24 in EC tissues compared with normal control tissues suggests miR-24 might play a role in tumorigenesis of EC. EC HEC-1A cells were transfected with miR-24 agonist (agomiR-24) to up-regulate the expression of miR-24. Up-regulation of miR-24 inhibited the cell proliferation and advanced the chemotherapy sensitivity to paclitaxel in HEC-1A cells significantly. We used several types of bioinformatic software to predict that miR-24 could specifically combine with the 3' untranslated region (3'UTR) of the S100A8 gene, and this prediction was verified by Western blot and luciferase activities assay. The regulation effects of miR-24 enhancement on cell proliferation and chemotherapy sensitivity were largely reversed by S100A8 up-regulation. CONCLUSIONS miR-24 acts as a tumor-suppressing gene to inhibit malignant proliferation and advance chemotherapy sensitivity to paclitaxel in EC by targeted silencing of the S100A8 gene.

No MeSH data available.


Related in: MedlinePlus