AFP acetylation promoted its oncogenic role by blocking binding to the phosphatase PTEN and the pro-apoptotic protein caspase-3, which increased signaling for proliferation, migration, and invasion and decreased apoptosis.
Transfection of miR-34a mimics upregulated the expression of phosphatase and tensin homolog (PTEN) in bladder cancer cells, and decreased cell migration and invasion. miR-34a may inhibit bladder cancer cell migration and invasion by upregulating PTEN. miR-34a may additionally serve as a potential therapeutic target for bladder cancer.
Up-regulation of miR-155 can promote the proliferation of NPC cells and inhibit cell apoptosis by targeting the PTEN-PI3K/AKT pathway, thereby participating in the development and invasion of NPC, indicating that it might be a potential novel target for treating NPC.
These findings indicate that Transgelin 2 promotes paclitaxel resistance and the migration and invasion of breast cancer by directly interacting with PTEN and activating the PI3K/Akt/GSK-3β pathway.
This mechanistic study revealed that ROCK1 significantly enhanced cell migration and invasion by inhibiting the phosphatase and tensin homolog (PTEN)/phosphoinositide 3‑kinase (PI3K)/FAK pathway.
Recuse assays showed that restoration of PTEN reversed the effects of miR-3691-5p on HCC cell migration and invasion through decreasing PI3K/Akt signaling.
Further studies revealed that miR-26a inhibited cell growth by repressing the methyltransferase EZH2 and promoted cell migration and invasion by inhibiting the phosphatase PTEN.
Therefore, circ_ORC2 binds with miR-19a and enhances its expression, thereby inhibiting downstream PTEN expression and activating Akt pathway to promote osteosarcoma cell growth and invasion.
Overexpression of TUSC8 promoted PTEN expression, and suppressed the invasion and migration of Hela cells, whereas miR-641 mimic treatment changed the effects.
In addition, miR-29a robustly promotes invasion in PTEN-deficient glioblastoma cells by repressing translation of the Sox4 transcription factor, and this upregulates the invasion-promoting protein, HIC5.
Additionally, the present study demonstrated that knockdown of PTEN in miR‑93‑5p‑depleted RB cells significantly reversed the effects of miR‑93‑5p on cell proliferation, migration and invasion; miR‑93‑5p knockdown was suggested to promote PTEN expression, consequently inhibiting the activation of phosphoinositide 3‑kinase (PI3K)/protein kinase B (AKT) signaling pathway.
In response to miR-494 mimic, MB cells were found to have increased Bax and PTEN expressions, as well as cell number in G1 phase and cell apoptosis and decreased c-myc, p38 MAPK, Bcl-2, MTDH, IL-6, and survivin expression and cell number count in the S phase, cell proliferation, migration, and invasion.
We found that in the presence of extracellular nucleotides cilia-dependent chemosensation of the nucleotides inhibited migration and invasion in normal ciliated cholangiocytes through a P2Y11 receptor and liver kinase B1 (LKB1)-phosphatase and tensin homolog-AKT-dependent mechanism.
Upregulation of miR-718 could increase PI3K/Akt signaling by directly downregulating PTEN, thus promoting the proliferation and invasion of gastric cancer cells.
In summary, our findings suggest that miR-222 plays an important role in promoting ovarian carcinoma cell invasion and migration and miR-222/PTEN may be a novel therapeutic target of miRNA-mediated promotion of cell invasion and migration in ovarian carcinoma.
PTBP1 exerts these effects, in part, by regulating the phosphatase and tensin homolog-phosphatidylinositol-4,5-bisphosphate 3-kinase/protein kinase B (PTEN-PI3K/Akt) pathway and autophagy, and consequently alters cell growth and contributes to the invasion and metastasis.