Exogenous OGF enhances the anti-tumor activity of cisplatin on hepatocellular carcinoma
Hepatocellular carcinoma results in high cancer mortality and is difficult to eradicate because of its late stage at the time of diagnosis, multicentricity, and cirrhotic background. It is therefore urgent to explore effective and economical therapeutic methods to treat this disease. We aimed to inv...
Gespeichert in:
Veröffentlicht in: | International journal of clinical and experimental pathology 2019-01, Vol.12 (2), p.590-598 |
---|---|
Hauptverfasser: | , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
Zusammenfassung: | Hepatocellular carcinoma results in high cancer mortality and is difficult to eradicate because of its late stage at the time of diagnosis, multicentricity, and cirrhotic background. It is therefore urgent to explore effective and economical therapeutic methods to treat this disease.
We aimed to investigate the antitumor activity of exogenous opioid growth factor (OGF), as well as the effect of the combination of OGF and cisplatin on hepatocellular carcinoma. The possible underlying mechanisms were also explored.
RT-PCR and immunohistochemistry were employed to determine the expression of OGF receptor (OGFr) in hepatocellular carcinoma. MTT assays were used to explore the effect of OGF on cell migration and proliferation. Animal experiments were performed to explore the effect of OGF and DDP on tumors.
OGFr is present in human HCC cells and was differentially expressed between HCC tumor and non-tumor tissues. OGF inhibited HCC cell proliferation and migration. The silencing of OGFr blocked the expression of p21 and p53. Treatment using OGF, DDP and OGF+DDP all suppressed the growth of HCC tumors, with the maximum effect in the OGF+DDP group.
Our study clarified that OGF inhibits cell migration and proliferation of HCC in animal experiments and that exogenous OGF enhances the anti-tumor activity of cisplatin on HCC by upregulating p21 and p53. These findings may provide a new strategy for future HCC therapeutics. |
---|---|
ISSN: | 1936-2625 |