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The MicroRNA-217 Functions as a Potential Tumor Suppressor in Gastric Cancer by Targeting GPC5.

Wang H, Dong X, Gu X, Qin R, Jia H, Gao J - PLoS ONE (2015)

Bottom Line: Enforced expression of miR-217 inhibited GC cells proliferation and invasion.Moreover, Glypican-5 (GPC5), a new ocncogene, was identified as the potential target of miR-217.In addition, overexpression of miR-217 impaired GPC5-induced promotion of proliferation and invasion in GC cells.

View Article: PubMed Central - PubMed

Affiliation: Department of Gastroenterology, The Affiliated YanAn Hospital of Kunming Medical University, Kunming, 650051, Yunnan, China.

ABSTRACT
Gastric cancer (GC) is one of the most common malignancies worldwide. Emerging evidence has shown that aberrant expression of microRNAs (miRNAs) plays important roles in cancer progression. However, little is known about the potential role of miR-217 in GC. In this study, we investigated the role of miR-217 on GC cell proliferation and invasion. The expression of miR-217 was down-regulated in GC cells and human GC tissues. Enforced expression of miR-217 inhibited GC cells proliferation and invasion. Moreover, Glypican-5 (GPC5), a new ocncogene, was identified as the potential target of miR-217. In addition, overexpression of miR-217 impaired GPC5-induced promotion of proliferation and invasion in GC cells. In conclusion, these findings revealed that miR-217 functioned as a tumor suppressor and inhibited the proliferation and invasion of GC cells by targeting GPC5, which might consequently serve as a therapeutic target for GC patients.

No MeSH data available.


Related in: MedlinePlus

miR-217 inhibits GC cell proliferation and invasion.(A) Real-time RT-PCR analysis of miR-217 in HGC-27 cells upon transfection ofmiR-217 mimic. The expression of miR-217 in HGC-27 cells transfected with miR-217 mimics was up-regulated.U6 snRNA was used as internal control. (B) The expression of miR-217 in HGC-27 cells transfected with miR-217inhibitor was down-regulated.U6 snRNA was used as internal control. (C) Ectopic miR‑217 expression significantly inhibited cell proliferation, as demonstrated by CCK8 assay. (D) Inhibition of miR-217 expression significantly promoted cell proliferation, as demonstrated by CCK8 assay. (E) Invasion analysis of HGC-27cells after treatment withmiR-217 mimics, inhibitors or scramble or control; the relative ratio of invasive cells per field is shown below, *p<0.05, ** p<0.01, and ***p<0.001.
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pone.0125474.g003: miR-217 inhibits GC cell proliferation and invasion.(A) Real-time RT-PCR analysis of miR-217 in HGC-27 cells upon transfection ofmiR-217 mimic. The expression of miR-217 in HGC-27 cells transfected with miR-217 mimics was up-regulated.U6 snRNA was used as internal control. (B) The expression of miR-217 in HGC-27 cells transfected with miR-217inhibitor was down-regulated.U6 snRNA was used as internal control. (C) Ectopic miR‑217 expression significantly inhibited cell proliferation, as demonstrated by CCK8 assay. (D) Inhibition of miR-217 expression significantly promoted cell proliferation, as demonstrated by CCK8 assay. (E) Invasion analysis of HGC-27cells after treatment withmiR-217 mimics, inhibitors or scramble or control; the relative ratio of invasive cells per field is shown below, *p<0.05, ** p<0.01, and ***p<0.001.

Mentions: The expression of miR-217was increased in transfected HGC-27 cells using miR-217 mimics (Fig 3A) and decreased using miR-217 inhibitor (Fig 3B). The proliferation was reduced in the HGC-27 cells transfected withmiR-217 mimics compared with cells transfected with scramble or untreated (Fig 3C). Meanwhile, the proliferation was increased in HGC-27 cells transfected withmiR-217inhibitor compared with cells transfected with control or untreated (Fig 3D). The invasiveness of cells transfected with miR-217 mimics was decreased compared with the scramble group or control group cells and miR-217 inhibitor increased cell invasion compared with the scramble group or control group cells (Fig 3E).


The MicroRNA-217 Functions as a Potential Tumor Suppressor in Gastric Cancer by Targeting GPC5.

Wang H, Dong X, Gu X, Qin R, Jia H, Gao J - PLoS ONE (2015)

miR-217 inhibits GC cell proliferation and invasion.(A) Real-time RT-PCR analysis of miR-217 in HGC-27 cells upon transfection ofmiR-217 mimic. The expression of miR-217 in HGC-27 cells transfected with miR-217 mimics was up-regulated.U6 snRNA was used as internal control. (B) The expression of miR-217 in HGC-27 cells transfected with miR-217inhibitor was down-regulated.U6 snRNA was used as internal control. (C) Ectopic miR‑217 expression significantly inhibited cell proliferation, as demonstrated by CCK8 assay. (D) Inhibition of miR-217 expression significantly promoted cell proliferation, as demonstrated by CCK8 assay. (E) Invasion analysis of HGC-27cells after treatment withmiR-217 mimics, inhibitors or scramble or control; the relative ratio of invasive cells per field is shown below, *p<0.05, ** p<0.01, and ***p<0.001.
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4476558&req=5

pone.0125474.g003: miR-217 inhibits GC cell proliferation and invasion.(A) Real-time RT-PCR analysis of miR-217 in HGC-27 cells upon transfection ofmiR-217 mimic. The expression of miR-217 in HGC-27 cells transfected with miR-217 mimics was up-regulated.U6 snRNA was used as internal control. (B) The expression of miR-217 in HGC-27 cells transfected with miR-217inhibitor was down-regulated.U6 snRNA was used as internal control. (C) Ectopic miR‑217 expression significantly inhibited cell proliferation, as demonstrated by CCK8 assay. (D) Inhibition of miR-217 expression significantly promoted cell proliferation, as demonstrated by CCK8 assay. (E) Invasion analysis of HGC-27cells after treatment withmiR-217 mimics, inhibitors or scramble or control; the relative ratio of invasive cells per field is shown below, *p<0.05, ** p<0.01, and ***p<0.001.
Mentions: The expression of miR-217was increased in transfected HGC-27 cells using miR-217 mimics (Fig 3A) and decreased using miR-217 inhibitor (Fig 3B). The proliferation was reduced in the HGC-27 cells transfected withmiR-217 mimics compared with cells transfected with scramble or untreated (Fig 3C). Meanwhile, the proliferation was increased in HGC-27 cells transfected withmiR-217inhibitor compared with cells transfected with control or untreated (Fig 3D). The invasiveness of cells transfected with miR-217 mimics was decreased compared with the scramble group or control group cells and miR-217 inhibitor increased cell invasion compared with the scramble group or control group cells (Fig 3E).

Bottom Line: Enforced expression of miR-217 inhibited GC cells proliferation and invasion.Moreover, Glypican-5 (GPC5), a new ocncogene, was identified as the potential target of miR-217.In addition, overexpression of miR-217 impaired GPC5-induced promotion of proliferation and invasion in GC cells.

View Article: PubMed Central - PubMed

Affiliation: Department of Gastroenterology, The Affiliated YanAn Hospital of Kunming Medical University, Kunming, 650051, Yunnan, China.

ABSTRACT
Gastric cancer (GC) is one of the most common malignancies worldwide. Emerging evidence has shown that aberrant expression of microRNAs (miRNAs) plays important roles in cancer progression. However, little is known about the potential role of miR-217 in GC. In this study, we investigated the role of miR-217 on GC cell proliferation and invasion. The expression of miR-217 was down-regulated in GC cells and human GC tissues. Enforced expression of miR-217 inhibited GC cells proliferation and invasion. Moreover, Glypican-5 (GPC5), a new ocncogene, was identified as the potential target of miR-217. In addition, overexpression of miR-217 impaired GPC5-induced promotion of proliferation and invasion in GC cells. In conclusion, these findings revealed that miR-217 functioned as a tumor suppressor and inhibited the proliferation and invasion of GC cells by targeting GPC5, which might consequently serve as a therapeutic target for GC patients.

No MeSH data available.


Related in: MedlinePlus