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MicroRNA‑197 reverses the drug resistance of fluorouracil‑induced SGC7901 cells by targeting mitogen‑activated protein kinase 1.

Xiong HL, Zhou SW, Sun AH, He Y, Li J, Yuan X - Mol Med Rep (2015)

Bottom Line: A luciferase reporter assay confirmed that miR‑197 led to silencing of the MAPK1 gene by recognizing and then specifically binding to the predicted site of the MAPK1 mRNA 3'‑untranslated region.When miR‑197 was overexpressed in SGC7901 cells, the protein levels of MAPK1 were downregulated.Furthermore, MAPK1 knockdown significantly increased the growth inhibition rate of the SGC7901/5‑FU cells compared with those in the control group.

View Article: PubMed Central - PubMed

Affiliation: Department of Medical Oncology, Huizhou Municipal Central Hospital of Guangdong Province, Huizhou, Guangdong 516000, P.R. China.

ABSTRACT
MicroRNAs (miRNAs) are a group of small non‑coding RNA molecules, which serve an important function in the development of multidrug resistance in cancer through the post‑transcriptional regulation of gene expression and RNA silencing. In the present study, the functional effects of miR‑197 were analyzed in chemo‑resistant gastric cancer cells. Low expression levels of miR‑197 were observed in the fluorouracil (5‑FU)‑resistant gastric cell line SGC7901/5‑FU when compared with those in the parental gastric cell line SGC7901. Overexpression of miR‑197 in SGC7901/5‑FU cells was identified to partially restore 5‑FU sensitivity. miRNA target prediction algorithms suggested that mitogen‑activated protein kinase 1 (MAPK1) is a candidate target gene for miR‑197. A luciferase reporter assay confirmed that miR‑197 led to silencing of the MAPK1 gene by recognizing and then specifically binding to the predicted site of the MAPK1 mRNA 3'‑untranslated region. When miR‑197 was overexpressed in SGC7901 cells, the protein levels of MAPK1 were downregulated. Furthermore, MAPK1 knockdown significantly increased the growth inhibition rate of the SGC7901/5‑FU cells compared with those in the control group. These results indicated that miR‑197 may influence the sensitivity of 5‑FU treatment in a gastric cancer cell line by targeting MAPK1.

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(A) Cell growth inhibition rate of SGC7901 and SGC7901/5-FU cells. (B) Expression levels of miR-197 in SGC7901 and SGC7901/5-FU cells. The cells were treated with various doses of 5-FU (0.5, 1.0, 2.0, 4.0 and 8.0 µmol/l). After 48 h of transfection, an MTT assay was performed to assess the growth inhibition rate of the cells.*P<0.05 vs. control. 5-FU, fluorouracil; miR-197, microRNA-197; SGC7901/5-FU, SGC7901 cell line resistant to 5-FU.
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f1-mmr-12-04-5019: (A) Cell growth inhibition rate of SGC7901 and SGC7901/5-FU cells. (B) Expression levels of miR-197 in SGC7901 and SGC7901/5-FU cells. The cells were treated with various doses of 5-FU (0.5, 1.0, 2.0, 4.0 and 8.0 µmol/l). After 48 h of transfection, an MTT assay was performed to assess the growth inhibition rate of the cells.*P<0.05 vs. control. 5-FU, fluorouracil; miR-197, microRNA-197; SGC7901/5-FU, SGC7901 cell line resistant to 5-FU.

Mentions: To detect the cell growth inhibition rate of the SGC7901/5-FU cell line and the parental SGC7901 cell line, an MTT assay was performed (Fig. 1A). The results demonstrated that compared with the SGC7901 cell line, the SGC7901/5-FU cells exhibited clear resistance to 5-FU. In order to determine the role of miR-197 in the 5-FU-resistant gastric cancer cell line SGC7901/5-FU, RT-qPCR analysis was conducted. The results indicated that miR-197 was downregulated in SGC7901/5-FU cells (Fig. 1B), which suggested that miR-197 may contribute to 5-FU drug resistance in gastric cancer cells.


MicroRNA‑197 reverses the drug resistance of fluorouracil‑induced SGC7901 cells by targeting mitogen‑activated protein kinase 1.

Xiong HL, Zhou SW, Sun AH, He Y, Li J, Yuan X - Mol Med Rep (2015)

(A) Cell growth inhibition rate of SGC7901 and SGC7901/5-FU cells. (B) Expression levels of miR-197 in SGC7901 and SGC7901/5-FU cells. The cells were treated with various doses of 5-FU (0.5, 1.0, 2.0, 4.0 and 8.0 µmol/l). After 48 h of transfection, an MTT assay was performed to assess the growth inhibition rate of the cells.*P<0.05 vs. control. 5-FU, fluorouracil; miR-197, microRNA-197; SGC7901/5-FU, SGC7901 cell line resistant to 5-FU.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4581796&req=5

f1-mmr-12-04-5019: (A) Cell growth inhibition rate of SGC7901 and SGC7901/5-FU cells. (B) Expression levels of miR-197 in SGC7901 and SGC7901/5-FU cells. The cells were treated with various doses of 5-FU (0.5, 1.0, 2.0, 4.0 and 8.0 µmol/l). After 48 h of transfection, an MTT assay was performed to assess the growth inhibition rate of the cells.*P<0.05 vs. control. 5-FU, fluorouracil; miR-197, microRNA-197; SGC7901/5-FU, SGC7901 cell line resistant to 5-FU.
Mentions: To detect the cell growth inhibition rate of the SGC7901/5-FU cell line and the parental SGC7901 cell line, an MTT assay was performed (Fig. 1A). The results demonstrated that compared with the SGC7901 cell line, the SGC7901/5-FU cells exhibited clear resistance to 5-FU. In order to determine the role of miR-197 in the 5-FU-resistant gastric cancer cell line SGC7901/5-FU, RT-qPCR analysis was conducted. The results indicated that miR-197 was downregulated in SGC7901/5-FU cells (Fig. 1B), which suggested that miR-197 may contribute to 5-FU drug resistance in gastric cancer cells.

Bottom Line: A luciferase reporter assay confirmed that miR‑197 led to silencing of the MAPK1 gene by recognizing and then specifically binding to the predicted site of the MAPK1 mRNA 3'‑untranslated region.When miR‑197 was overexpressed in SGC7901 cells, the protein levels of MAPK1 were downregulated.Furthermore, MAPK1 knockdown significantly increased the growth inhibition rate of the SGC7901/5‑FU cells compared with those in the control group.

View Article: PubMed Central - PubMed

Affiliation: Department of Medical Oncology, Huizhou Municipal Central Hospital of Guangdong Province, Huizhou, Guangdong 516000, P.R. China.

ABSTRACT
MicroRNAs (miRNAs) are a group of small non‑coding RNA molecules, which serve an important function in the development of multidrug resistance in cancer through the post‑transcriptional regulation of gene expression and RNA silencing. In the present study, the functional effects of miR‑197 were analyzed in chemo‑resistant gastric cancer cells. Low expression levels of miR‑197 were observed in the fluorouracil (5‑FU)‑resistant gastric cell line SGC7901/5‑FU when compared with those in the parental gastric cell line SGC7901. Overexpression of miR‑197 in SGC7901/5‑FU cells was identified to partially restore 5‑FU sensitivity. miRNA target prediction algorithms suggested that mitogen‑activated protein kinase 1 (MAPK1) is a candidate target gene for miR‑197. A luciferase reporter assay confirmed that miR‑197 led to silencing of the MAPK1 gene by recognizing and then specifically binding to the predicted site of the MAPK1 mRNA 3'‑untranslated region. When miR‑197 was overexpressed in SGC7901 cells, the protein levels of MAPK1 were downregulated. Furthermore, MAPK1 knockdown significantly increased the growth inhibition rate of the SGC7901/5‑FU cells compared with those in the control group. These results indicated that miR‑197 may influence the sensitivity of 5‑FU treatment in a gastric cancer cell line by targeting MAPK1.

Show MeSH
Related in: MedlinePlus