Mesenchymal stem cells (MSCs) in tumors have emerged as progenitors involved in stroma formation and metastasis of cancers, partially owing to their abilities to differentially express paracrine factors related to the proliferation and invasion of cancer cells. In this regard, increasing evidence has shown that MSCs have impacts on the malignancy of colon cancer, however, the underpinning mechanisms by which MSCs promote cancer metastasis remain elusive. To investigate the crosstalk between adipose-derived MSCs (AMSCs) isolated from adipose tissues and colon cancer cells, a co-culture transwell model of AMSCs and colon cancer cells was employed, and the activation of Wnt signaling and paracrine factors in colon cancer cells and AMSCs were measured. The results showed that AMSCs could enhance the metastatic capacity of colon cancer cells with an elevated expression of mesenchymal-epithelial transition (EMT)-associated genes in a contact-dependent manner. Reciprocally, colon cancer cells were able to induce AMSCs to produce metastasis-related factors and cytokines, such as FGF10, VEGFC and matrix metalloproteinases (MMPs) in part through a mechanism of an activation of Wnt signaling, by which these factors in turn activate Wnt signaling of colon cancer cells. Intriguingly, an inhibition of Wnt signaling leads a reduced capacity of invasion and colony formation of colon cancer cells in vitro, and the tumorigenicity of cancer cells in a murine model. These findings thus suggest that the crosstalk between the Wnt signaling of cancer cells and paracrine factors of AMSCs has an implication in colon cancer malignancy. This study thus uncovers a novel Wnt-paracrine factors mediated-crosstalk between colon cancer cells and AMSCs in cancer malignancy.

Astrocytic function imbalance is a key factor affecting cerebral ischemia rehabilitation. Mesenchymal stem cells have therapeutic potential for cerebral ischemia, but their mechanisms remain unclear. This study explored how placental mesenchymal stem cells pro-mote astrocytes towards the A2 phenotype, which benefits the repair of cerebral ischemia injury. We established the animal model of middle cerebral artery ischemia/reperfusion and an in vitro interleukin-1β-treated astrocyte inflammation model and utilized neuro-logical function assessment, 2,3,5-triphenyltetrazolium chloride staining, immunofluorescence staining, Western blotting and other methods to evaluate the impact and associated mechanisms of transplanting placental mesenchymal stem cells into rats with cerebral ischemia–reperfusion injuries. The results demonstrated that transplantation of placental mesenchymal stem cells ameliorated neurological dysfunction and histopathological damage, alleviated neuroinflammation and enhanced neurotrophic factor levels, promoted the polarization of interleukin-1β-treated astrocytes toward the A2 phenotype, and suppressed the abundance of core mediators within the cerebral TGF β1/Smad signaling cascade in ischemia/reperfusion model. Collectively, placental mesenchymal stem cell grafting facilitates the polarization of cerebral astrocytes toward the protective A2 phenotype, presumably by regulating the TGF β1/Smad signaling cascade in ischemic brain injury.