In conclusion, ectopic expression of miR-19a-3p contributes to HCC metastasis and chemoresistance by modulating PTEN expression and the PTEN-dependent pathways.
The miR-520/372/373 family targeted the SPOP 3'-UTR and suppressed SPOP protein expression, leading to elevation of PTEN and DUSP7 levels and, consequently, decreased proliferation, invasion/migration, and metastasis of RCC cells <i>in vitro</i> and <i>in vivo</i>.
Taken together, our findings suggest that functional interaction between Plac1 and Furin enhances breast cancer invasion and metastasis and the Furin/NICD/PTEN axis may act as an important therapeutic target for breast cancer treatment.
Lack of PTEN expression is associated with worsened overall survival, a more advanced Fuhrman grade, and a greater likelihood of lymph mode metastasis.
It is also characterized by reduced or absence of phosphatase and tensin homolog (PTEN) expression, a tumor suppressor gene having diverse functions including regulation of apoptosis, cell cycle, and metastasis.
NLRP3 in human glioma is correlated with increased WHO grade, and regulates cellular proliferation, apoptosis and metastasis via epithelial-mesenchymal transition and the PTEN/AKT signaling pathway.
When accounting for clinical information about the patient's cancer, the status of the PTEN gene alone matched a multigene panel to predict which patient's cancer would metastasize or lead to death from the disease.
Chemerin upregulated expression and phosphatase activity of PTEN by interfering with PTEN-CMKLR1 interaction, leading to weakened ubiquitination of PTEN and decreased p-Akt (Ser473) level, which was responsible for suppressed migration, invasion and metastasis of HCC cells.
Mechanistically, further analysis demonstrated that the effects of miR-616-3p on metastasis and angiogenesis occurred through the down-regulation of PTEN, a direct target of miR-616-3p.
Collectively, our data identified a tumor inducer, SYNJ2BP, which could activate the PI3K/AKT/GSK3β/SNAI1 signaling pathway through the lysosome-mediated degradation of PTEN, and promote both EMT and tumor metastasis during the progression of breast cancer.
Furthermore, gain- and loss-of-function studies of the phosphatase and tensin homolog (PTEN) were performed to assess whether the effect of miR-92a promoted growth and metastasis of NSCLC cells were via targeting PTEN.
Conversely, PTEN protein expression was markedly lower in CRC compared with adjacent normal tissues. p‑4E‑BP1 protein upregulation tissues samples was consistent with PTEN downregulation in CRC samples. p‑4E‑BP1 overexpression was predominant in patients with metastasis to the regional lymph nodes.
With the increase of FIGO (International Federation of Gynecology and Obstetrics) stage and depth of invasion, as well as the metastasis of pelvic lymph nodes, the expression levels of TFF-1 and PTEN mRNAs were significantly decreased, and the differences were statistically significant (p < 0.05).
CCAT2 was an endogenous sponge by competing for miR-216b, and miR-216b suppression alleviated CCAT2 silence-diminished cell growth and metastasis. miR-216b negatively regulated Bcl-2 and Bcl-2 could further active PTEN/PI3K/AKT and mTOR signaling pathways.
PTEN expression was significantly correlated with gender, smoking history, histology (adenocarcinoma [ADC] vs. squamous cell carcinoma), tumor node metastasis stage (I-II vs. III-IV), N status (N0 vs. N1-N3), and distant metastasis (M0 vs. M1).
Among patients without distant metastases (n = 282), a high pretreatment PTEN mRNA level was associated with inferior relapse-free (RFS; p = 0.001) and disease-specific survival (DSS; p = 0.003).
Most interestingly, in vivo studies indicated that miR-205 markedly promoted the growth and metastasis of tumors and the expression of miR-205 was also found to be inversely correlated with that of SMAD4 and PTEN in nude mice.
Our findings indicate that NEDD4 potentially plays a critical role in activating the PI3K/AKT signaling pathway by negatively regulating PTEN levels in PDAC cells, which promotes pancreatic cancer cell proliferation and metastasis.
In MKN-28 cells, PTEN was suppressed by miR-26a through 3'-UTR, and PTEN mediated miR-26a promoting oncogenicity including cell proliferation and metastasis.