FGF6

Official Full Name

fibroblast growth factor 6

Organism

Homo sapiens

GeneID

2251

Background

The protein encoded by this gene is a member of the fibroblast growth factor (FGF) family. FGF family members possess broad mitogenic and cell survival activities, and are involved in a variety of biological processes, including embryonic development, cell growth, morphogenesis, tissue repair, tumor growth and invasion. This gene displayed oncogenic transforming activity when transfected into mammalian cells. The mouse homolog of this gene exhibits a restricted expression profile predominantly in the myogenic lineage, which suggested a role in muscle regeneration or differentiation. [provided by RefSeq, Jul 2008]

Synonyms

HST2; HBGF-6;

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Detailed Information

Fibroblast growth factor (FGF) is a multi-gene family that plays an important role in promoting a variety of physiological and pathological processes, such as embryo development, tissue repair, neuroprotection, tumor genesis, and metastasis. FGFs consist of 23 members with molecular weights ranging from 17×10³ to 34×10³, and all the FGFs have a conserved core consisting of 120 amino acids. According to the sequence homology and phylogenetic differences, these families can be divided into three types, including parasecretory FGF, endocrine FGF, and cytosecretory FGF. FGF6, as one of its family members, is mainly expressed in skeletal muscle tissue. In addition, FGF6 can not only promote muscle regeneration but also accelerate the proliferation and differentiation of muscle cells, exhibiting its potential clinical value. FGF6 has also been found to be expressed in the muscles of the mouth, tongue, pharynx, and neck. In adult testes, FGF6 transcripts have also been detected, but the important role of FGF6 in human prostate cancer needs to be further studied. Other studies have found that FGF6 can promote the proliferation of cardiomyocytes and protect cardiomyocytes from apoptosis. In conclusion, FGF6 has a variety of biological functions in angiogenesis, bone formation, tongue development, and other aspects.

Muscle regeneration enhanced by FGF6

Skeletal muscle injury is one of the most common injuries in sports medicine. The study of skeletal muscle repair and regeneration is of great clinical significance in the field of treatment and rehabilitation after skeletal muscle injury. The skeletal muscle that is damaged severely has remarkable regenerative capacity. Skeletal muscle regeneration is maintained by satellite cells. The satellite cells of mature skeletal muscle are normally stationary but they become activated after injury. The relative research has shown that FGF6 of wild-type mice will be up-regulated after skeletal muscle injury, which promotes a complete recovery of the experimentally damaged skeletal muscle. The protective effect on skeletal muscle and the effect on the proliferation and differentiation due to the change of FGF6 expression has been studied by Wu’s group. They demonstrated that the viability and migration of C2C12 have been promoted by FGF6. FGF6 at Low concentrations has promoted myoblast differentiation through the activation of ERK1/2 mediated by FGFR4. These results indicated that skeletal muscle atrophy was reduced by FGF6 based on the ERK1/2 mechanism, and the conversion from slow muscle to fast muscle fibers has been further enhanced by FGF6, thereby promoting the good recovery of regenerated skeletal muscle.

FGF6 associated with early mouse tongue development

The tongue is one of the highly flexible organs that is important for multiple human actions, such as speaking, chewing, and swallowing. FGF signaling is reported to play a vital role in tongue development by Klein’s group. They have demonstrated that FGF6 controls myoblast differentiation and myoblast fusion during tongue development. They have also investigated the expression of different FGF members during early tongue development, including FGF5-7, FGF9, Fgf10, Fgf16, and Fgf18. It is shown that the expression of FGF6 was at low levels in E11.5 and E12.5, but it was significantly up-regulated from E13.5, suggesting the great function of FGF6 in the tongue differentiation period. All the results have given powerful evidence that FGF6 can act as a downstream of TGFβ signaling mediated by SMAD4 to control myoblast differentiation and myoblast fusion during tongue myogenesis.

FGF6 Figure 1. Scheme model for explaining the mechanism of FGF6/FGF9-mediated Ucp1 expression (Shamsi et al., 2020).

References:

Cai Q, Wu G, Zhu M, et al. FGF6 enhances muscle regeneration after nerve injury by relying on ERK1/2 mechanism[J]. Life sciences, 2020, 248: 117465.
Du W, Prochazka J, Prochazkova M, et al. Expression of FGFs during early mouse tongue development[J]. Gene Expression Patterns, 2016, 20(2): 81-87.
Shamsi F, Xue R, Huang T L, et al. FGF6 and FGF9 regulate UCP1 expression independent of brown adipogenesis[J]. Nature communications, 2020, 11(1): 1-16.

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