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Microvascular invasion in hepatocellular carcinoma overexpression promotes cell proliferation and inhibits cell apoptosis of hepatocellular carcinoma via inhibiting miR-199a expression.

Shi Y, Song Q, Yu S, Hu D, Zhuang X - Onco Targets Ther (2015)

Bottom Line: MVIH expression was significantly increased and miR-199a expression was significantly decreased in tumor tissue and HCC cells. si-MVIH inhibited HCC cell viability and promoted cell apoptosis, but this effect was reversed by miR-199a inhibitor.Luciferase reporter assay and RNA immunoprecipitation experiment showed that miR-199a had a direct binding ability to MVIH RNA.MVIH promoted cell growth and inhibited cell apoptosis of HCC via inhibiting miR-199a expression.

View Article: PubMed Central - PubMed

Affiliation: Department of General Surgery, Affiliated Hospital of Xuzhou Medical College, Xuzhou, People's Republic of China.

ABSTRACT

Objectives: Long non-coding RNA (lncRNA) associated with microvascular invasion in hepatocellular carcinoma (MVIH) has been recently reported to act as a predictor for the poor recurrence-free survival of hepatocellular carcinoma (HCC) after hepatectomy. However, the biological role of MVIH in the tumorigenesis of HCC is still unclear.

Methods: In the study reported here, MVIH expression levels were detected by real-time polymerase chain reaction (PCR) in tumor tissue of HCC patients and in HCC cells, including SMMC7721 and HepG2 cells. Cell viability and apoptosis were determined by MTT and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) methods, respectively. The model of transplantation tumor of HepG2 cells in nude mice was used to evaluate the effects of MVIH and miR-199a on HCC in vivo.

Results: MVIH expression was significantly increased and miR-199a expression was significantly decreased in tumor tissue and HCC cells. si-MVIH inhibited HCC cell viability and promoted cell apoptosis, but this effect was reversed by miR-199a inhibitor. Luciferase reporter assay and RNA immunoprecipitation experiment showed that miR-199a had a direct binding ability to MVIH RNA. In nude mice with transplantation, the tumor volume was reduced by si-MVIH, and miR-199a inhibitor canceled this decrease.

Conclusion: MVIH promoted cell growth and inhibited cell apoptosis of HCC via inhibiting miR-199a expression.

No MeSH data available.


Related in: MedlinePlus

Downregulation of microvascular invasion in hepatocellular carcinoma (MVIH) inhibits cell viability and promotes cell apoptosis of hepatocellular carcinoma cells. siRNA-MVIH was transfected into hepatocellular carcinoma cells (HepG2 and SMMC7721) for 48 hours and then the miR-199a inhibitor or negative control (NC) was transfected into hepatocellular carcinoma cells for another 48 hours. The cell viability was detected by MTT assay (A); the cell apoptosis was measured by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) method (B).Notes: *P<0.05, versus with cells transfected with si-MVIH; #P<0.05, versus with cells transfected with si-MVIH and NC.
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f2-ott-8-2303: Downregulation of microvascular invasion in hepatocellular carcinoma (MVIH) inhibits cell viability and promotes cell apoptosis of hepatocellular carcinoma cells. siRNA-MVIH was transfected into hepatocellular carcinoma cells (HepG2 and SMMC7721) for 48 hours and then the miR-199a inhibitor or negative control (NC) was transfected into hepatocellular carcinoma cells for another 48 hours. The cell viability was detected by MTT assay (A); the cell apoptosis was measured by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) method (B).Notes: *P<0.05, versus with cells transfected with si-MVIH; #P<0.05, versus with cells transfected with si-MVIH and NC.

Mentions: To investigate the role of MVIH in HCC, cells were transfected with si-MVIH to downregulate MVIH expression. The results showed that si-MVIH significantly inhibited the cell viability of HepG2 and SMMC7721 cells (Figure 2A and B), while markedly promoted the cell apoptosis (Figure 2C and D). HCC cells supplemented with miR-199a inhibitor, the decrease of cell viability and increase of cell apoptosis induced by si-MVIH were reversed.


Microvascular invasion in hepatocellular carcinoma overexpression promotes cell proliferation and inhibits cell apoptosis of hepatocellular carcinoma via inhibiting miR-199a expression.

Shi Y, Song Q, Yu S, Hu D, Zhuang X - Onco Targets Ther (2015)

Downregulation of microvascular invasion in hepatocellular carcinoma (MVIH) inhibits cell viability and promotes cell apoptosis of hepatocellular carcinoma cells. siRNA-MVIH was transfected into hepatocellular carcinoma cells (HepG2 and SMMC7721) for 48 hours and then the miR-199a inhibitor or negative control (NC) was transfected into hepatocellular carcinoma cells for another 48 hours. The cell viability was detected by MTT assay (A); the cell apoptosis was measured by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) method (B).Notes: *P<0.05, versus with cells transfected with si-MVIH; #P<0.05, versus with cells transfected with si-MVIH and NC.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4556036&req=5

f2-ott-8-2303: Downregulation of microvascular invasion in hepatocellular carcinoma (MVIH) inhibits cell viability and promotes cell apoptosis of hepatocellular carcinoma cells. siRNA-MVIH was transfected into hepatocellular carcinoma cells (HepG2 and SMMC7721) for 48 hours and then the miR-199a inhibitor or negative control (NC) was transfected into hepatocellular carcinoma cells for another 48 hours. The cell viability was detected by MTT assay (A); the cell apoptosis was measured by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) method (B).Notes: *P<0.05, versus with cells transfected with si-MVIH; #P<0.05, versus with cells transfected with si-MVIH and NC.
Mentions: To investigate the role of MVIH in HCC, cells were transfected with si-MVIH to downregulate MVIH expression. The results showed that si-MVIH significantly inhibited the cell viability of HepG2 and SMMC7721 cells (Figure 2A and B), while markedly promoted the cell apoptosis (Figure 2C and D). HCC cells supplemented with miR-199a inhibitor, the decrease of cell viability and increase of cell apoptosis induced by si-MVIH were reversed.

Bottom Line: MVIH expression was significantly increased and miR-199a expression was significantly decreased in tumor tissue and HCC cells. si-MVIH inhibited HCC cell viability and promoted cell apoptosis, but this effect was reversed by miR-199a inhibitor.Luciferase reporter assay and RNA immunoprecipitation experiment showed that miR-199a had a direct binding ability to MVIH RNA.MVIH promoted cell growth and inhibited cell apoptosis of HCC via inhibiting miR-199a expression.

View Article: PubMed Central - PubMed

Affiliation: Department of General Surgery, Affiliated Hospital of Xuzhou Medical College, Xuzhou, People's Republic of China.

ABSTRACT

Objectives: Long non-coding RNA (lncRNA) associated with microvascular invasion in hepatocellular carcinoma (MVIH) has been recently reported to act as a predictor for the poor recurrence-free survival of hepatocellular carcinoma (HCC) after hepatectomy. However, the biological role of MVIH in the tumorigenesis of HCC is still unclear.

Methods: In the study reported here, MVIH expression levels were detected by real-time polymerase chain reaction (PCR) in tumor tissue of HCC patients and in HCC cells, including SMMC7721 and HepG2 cells. Cell viability and apoptosis were determined by MTT and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) methods, respectively. The model of transplantation tumor of HepG2 cells in nude mice was used to evaluate the effects of MVIH and miR-199a on HCC in vivo.

Results: MVIH expression was significantly increased and miR-199a expression was significantly decreased in tumor tissue and HCC cells. si-MVIH inhibited HCC cell viability and promoted cell apoptosis, but this effect was reversed by miR-199a inhibitor. Luciferase reporter assay and RNA immunoprecipitation experiment showed that miR-199a had a direct binding ability to MVIH RNA. In nude mice with transplantation, the tumor volume was reduced by si-MVIH, and miR-199a inhibitor canceled this decrease.

Conclusion: MVIH promoted cell growth and inhibited cell apoptosis of HCC via inhibiting miR-199a expression.

No MeSH data available.


Related in: MedlinePlus