<b>Conclusion:</b> Our results demonstrated that miR-3691-5p contributes to HCC cell migration and invasion through activating PI3K/Akt signaling by targeting PTEN.
Invasion responses were positively correlated with phosphorylation of phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) and p42/p44 mitogen-activated protein kinase (ERK).
PI3K/Akt signaling pathway emerges as a common pathway regulating cellular proliferation, migration and invasion; however, its contribution to particular process and downstream cascades remain poorly defined.
PI3k/Akt inhibitor inhibited the function of the macrophage in promoting cell proliferation and invasion of colon cancer through down-regulating paxillin.
Activation of PI3K/Akt and Erk, kinases related to actin cytoskeleton rearrangement and phagocytosis, reinforces the idea that T. cruzi EA subverts the phagocytic machinery during invasion.
Activation of the PI3k-Akt pathway by ATRA promotes invasion through Rac-GTPase, whereas pretreatment with 15e (PI3k inhibitor) or over-expression of the inactive form of Akt blocks ATRA-induced invasion.
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.
After SCC transformation, the absence of G45 domain in DeltaG45 cells was associated with deficient extracellular signal-regulated kinase and phosphotidylinositol 3-kinase (PI3K) pathway activation, impaired invasion, deficient metalloproteinase activity, and absent tumorgenicity in vivo.
Also, silencing of CAV2 inhibited the proliferation, migration and invasion, as well as the expression of EGFR, PI3K and p-Akt in OS-RC-2 cells in vitro, and OS-RC-2 xenograft growth in vivo.
An EGF receptor (EGFR) kinase inhibitor, a RasN17 dominant-negative construct, MEK and PI3K inhibitors significantly blocked EGF/EGFR-stimulated MMP-9, cell invasion, and colony formation in U1242 MG cells, suggesting that MMP-9 is involved in EGFR/Ras/MEK and PI3K/AKT signaling pathway-mediated cell invasion and anchorage-independent growth in U1242 MG cells.
Analysis of the predominant intracellular signaling pathways that act downstream of the activated CXCR4/CXCL12 axis, namely the phosphatidyl inositol 3‑kinase (PI3K)‑protein kinase B (Akt) cascades, revealed that RSG rapidly interferes with the phosphorylation/activation of Akt, which mediates CXCL12‑stimulated migration and invasion.
And miR-206 downregulation impaired the suppressive effects of cZNF292 silence toward Eca-109 cell growth, migration, and invasion. cZNF292 silencing activated AMPK signaling and inactivated PI3K/AKT signaling also via regulating miR-206.
As a member of granulin superfamily, CsGRN induced mesenchymal characteristics of PLC and RBE cells and was found to regulate the activities of the downstream molecules of the ERK and PI3K/AKT signalling pathways, which could contribute to the enhancement of cell migration and invasion.