At the present study, we found overexpression of <i>miR-141</i> could inhibit proliferation, migration, tumor-forming and invasive potential of CRC cells <i>in vitro</i> and mitogen-activated protein kinase kinase kinase kinase 4 (MAP4K4) was verified as a directed target of <i>miR-141</i> The combination treatment of <i>miR-141</i> with 5-FU, directly targetting MAP4K4, could better inhibit invasion and metastasis of CRC cells colony than either one alone.
The parallel increase of c-Met and MAP4K4 expression in SHH MB could predict an increased potential of these tumors to infiltrate brain tissue and cause metastatic disease.
Knockdown of MAP4K4 inhibited proliferation, anchorage-independent growth and migration of lung adenocarcinoma cells, and also inhibited human lung adenocarcinoma xenograft growth and metastasis.
Using the specific 185-gene signature generated by unsupervised consensus clustering of gene expression data, we defined four subtypes associated with distinct clinical metrics: tumors with high metastasis associated with EMT (epithelial to mesenchymal transition) and active MAP4K4/JNK signaling pathway; tumors with high chromosomal instability with up regulated MYC targes; well differentiated tumors with less aggressive and moderated tumors.
Furthermore, microarray analysis revealed that PRR11 knockdown caused the dysregulation of multiple critical pathways and various important genes involved in cell cycle, tumorigenesis and metastasis (e.g.CCNA1, RRM1, MAP4K4 and EPB41L3).
The high metastatic potential of melanoma cells was prevented by the HGK motif in the P-5m peptide in vitro and in an experimental lung metastasis model, suggesting that P-5m may play an important role in the regulation of tumor metastasis.