Far beyond anti-angiogenesis: Benefits for anti-basicFGF therapy in cancer

Role of Basic Fibroblast Growth Factor in Cancer: Biological Activity, Targeted Therapies, and Prognostic Value

“…These data pave the way for a new RNA splicing-dependent mechanism by which bFGF initiates blood vessel formation. Confirming this, a correlation was found between bFGF and sVEGFR1 in patients with squamous lung cancer [ 39 ]. Furthermore, since bFGF and VEGF promote angiogenesis by contributing to tumor growth and spread, they have been widely associated with shorter overall survival in non-small cell lung cancer patients [ 46 ], as well as in subjects affected by hepatocellular carcinoma and non-Hodgkin lymphoma [ 47 , 48 ].…”

“…bFGF was discovered as a typical inducer of angiogenesis, and it has already been studied for three decades. Recent evidence indicates that bFGF plays different roles and controls signaling pathways, and it identifies bFGF’s typical role in angiogenesis [ 39 ]. bFGF represents a typically pro-angiogenic factor and is certainly the most distinguished in the large family of FGFs, being present in sites of chronic inflammation, tissue damage, etc.…”

“…It is known that bFGF can also influence the metabolism of vascular endothelial cells by overregulating HK2, through which it monitors the glycolytic process and thus promotes angiogenesis [ 45 ]. Furthermore, it is important to underline the PLCγ/IP3/Ca 2+ signaling as another canonical signaling pathway induced by FGF/FGFR, leading to the activation of PKC, an important regulating factor in angiogenesis [ 39 ].…”

“…Recently, a new study indicated that bFGF induces the expression of the splice factors SRSF1 and SRSF3 and the splice kinase SRPK1 in the HUVEC and HDMEC endothelial cell lines by modulating the splicing of the vascular endothelial growth factor 1 (VEGFR1) receptor towards splice variants known as soluble VEGFR1 (sVEGFR1), which are devoid of their transmembrane and intracellular segments [ 39 ]. These data pave the way for a new RNA splicing-dependent mechanism by which bFGF initiates blood vessel formation.…”

MSC based gene delivery methods and strategies improve the therapeutic efficacy of neurological diseases

“…Because the gene expression profile of MSCs modified by different genes will change dramatically, especially the activation of some uncontrolled signaling pathways brings concerns about their safety. For the gene modification strategies that promote cell proliferation or survival under stress, their safety is more worthy of attention, because in many tumor tissues, the expression of these genes is also abnormal, such as bFGF, Bcl2, etc [ 323 , 324 ]. Although the overexpression of these genes promoted the survival rate of MSCs in local transplantation, it also brought a certain risk of tumor development.…”