Taken together, our results suggest that THOR could promote HCC cell growth and metastasis by amplifying PTEN/AKT signaling and may be a new therapeutic target and predictive factor for HCC.
An inverse correlation between miR-32-5p and PTEN was confirmed in HCC cell lines and patients; moreover, high expression of miR-32-5p and low expression of PTEN were positively associated with poor prognosis.
In contrast, Kras activation in combination with heterozygous PTEN deletion induced mixed carcinomas of liver (both ICC and hepatocellular carcinoma, HCC), whereas Kras activation alone did not induce biliary tract neoplasm.
Mechanistic studies suggested that immune response, PI3K/AKT/mTOR/PTEN pathway, mitochondrial dysfunction and genetic alterations are important mediators in the progression of NAFLD-HCC from metabolic disorder.
It was also be found that ONTD increase the PPAR-γ activity, reduce the phosphorylation of Akt and increase phosphatase and tensin homologue (PTEN) protein expression in hepatocellular carcinoma (HCC) Bel-7402 cells, and these were associated with the inhibition of cells proliferation.
In this study, we investigated the expression status of SALL4, HDAC1, and HDAC2 and their relationship with phosphatase and tensin homolog deleted on chromosome 10 (PTEN) by immunohistochemical analysis of the posthepatectomy specimens of 135 patients with hepatocellular carcinoma who were treated at our hospital.
Alterations in this pathway, as well as in TP53 and the cell cycle machinery, and in the PI3K/Akt/mTor axis (the latter activated in the presence of PTEN loss), as well as aberrant angiogenesis and epigenetic anomalies, appear to be major events in HCC.
Finally, HBx interrupted the balance between apoptosis and proliferation, which contributed to the development of hepatocellular carcinoma, was also related to the interaction of miR-181a and PTEN.
Therefore, authors introduced new integration between gene therapy and nanotechnology in the form of PTEN and TRAIL-loaded ZNPs that proved potential to be used in gene therapy for the treatment of HCC.
The present study investigated the oncogenic role of NEDD4 in hepatocellular carcinoma (HCC) by targeted small interfering RNA silencing of the tumor suppressor phosphatase and tensin homolog (PTEN).
Hepatitis B virus X protein increases microRNA‑21 expression and accelerates the development of hepatoma via the phosphatase and tensin homolog/phosphoinositide 3‑kinase/protein kinase B signaling pathway.
Through in vitro experiments, we found that miR-155-5p promoted proliferation, invasion and migration, but inhibited apoptosis in HCC by directly targeting the 3'-UTR of PTEN.
Downregulation of AZGP1 by Ikaros and histone deacetylase promotes tumor progression through the PTEN/Akt and CD44s pathways in hepatocellular carcinoma.
Taken together, we found that FR5 effectively inhibits proliferation and induces apoptosis of HCC cells through coordinated inhibition of YAP in the Hippo pathway and AKT in the PI3K-PTEN-mTOR pathway, and suggest FR5 as a potential therapy for HCC.
However, the precise effects mediated by PTENP1 transcripts within intricate regulatory networks involving molecular interactions with PTEN and tumorigenicity in hepatocellular carcinoma (HCC) remains elusive.
This suggests that the loss of PTEN might occur both in HA and HCC, constituting different outcomes of the same molecular lesion in the various contexts of malignant or benign neoplasms.
Meanwhile, EPAP enhanced gene expression and cellular uptake in HepG2 cells, and showed significant inhibition in cell proliferation and cell migration against hepatocellular carcinoma cells HepG2 while showing no cytotoxicity to normal liver cells L-02, compared with Ad5-PTEN.