Limits...
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

The microvascular invasion in hepatocellular carcinoma (MVIH) and miR-199a expression in hepatocellular carcinoma (HCC) tissue and cells. The relative MVIH and miR-199a expression levels were quantified by real-time polymerase chain reaction (PCR) in HCC tissue (n=15, A) and cells (n=3, B).Note: **P<0.01, versus normal tissue or normal hepatocyte HL-7702 cells.
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4556036&req=5

f1-ott-8-2303: The microvascular invasion in hepatocellular carcinoma (MVIH) and miR-199a expression in hepatocellular carcinoma (HCC) tissue and cells. The relative MVIH and miR-199a expression levels were quantified by real-time polymerase chain reaction (PCR) in HCC tissue (n=15, A) and cells (n=3, B).Note: **P<0.01, versus normal tissue or normal hepatocyte HL-7702 cells.

Mentions: MVIH and miR-199a expression was detected by real-time PCR. As shown in Figure 1A, the MVIH level in HCC tissue was 3.75-fold than that of normal tissue, and the miR-199a level was 0.39-fold than that of normal tissue. The MVIH and miR-199a expression levels were also detected in HCC cells. As indicated in Figure 1B, SMMC7721 and HepG2 HCC cells had a higher expression of MVIH and lower expression of miR-199a compared with normal hepatocyte HL-7702 cells.


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)

The microvascular invasion in hepatocellular carcinoma (MVIH) and miR-199a expression in hepatocellular carcinoma (HCC) tissue and cells. The relative MVIH and miR-199a expression levels were quantified by real-time polymerase chain reaction (PCR) in HCC tissue (n=15, A) and cells (n=3, B).Note: **P<0.01, versus normal tissue or normal hepatocyte HL-7702 cells.
© Copyright Policy
Related In: Results  -  Collection

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

f1-ott-8-2303: The microvascular invasion in hepatocellular carcinoma (MVIH) and miR-199a expression in hepatocellular carcinoma (HCC) tissue and cells. The relative MVIH and miR-199a expression levels were quantified by real-time polymerase chain reaction (PCR) in HCC tissue (n=15, A) and cells (n=3, B).Note: **P<0.01, versus normal tissue or normal hepatocyte HL-7702 cells.
Mentions: MVIH and miR-199a expression was detected by real-time PCR. As shown in Figure 1A, the MVIH level in HCC tissue was 3.75-fold than that of normal tissue, and the miR-199a level was 0.39-fold than that of normal tissue. The MVIH and miR-199a expression levels were also detected in HCC cells. As indicated in Figure 1B, SMMC7721 and HepG2 HCC cells had a higher expression of MVIH and lower expression of miR-199a compared with normal hepatocyte HL-7702 cells.

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