Abstract
Krüppel-like factor 10 (KLF10), originally named TGF-β (Transforming growth factor beta) inducible early gene 1 (TIEG1), is a DNA-binding transcriptional regulator containing a triple C2H2 zinc finger domain. By binding to Sp1 (specificity protein 1) sites on the DNA and interactions with other regulatory transcription factors, KLF10 encourages and suppresses the expression of multiple genes in many cell types. Many studies have investigated its signaling cascade, but other than the TGF-β/Smad signaling pathway, these are still not clear. KLF10 plays a role in proliferation, differentiation as well as apoptosis, just like other members of the SP (specificity proteins)/KLF (Krüppel-like Factors). Recently, several studies reported that KLF10 KO (Knock out) is associated with defects in cell and organs such as osteopenia, abnormal tendon or cardiac hypertrophy. Since KLF10 was first discovered, several studies have defined its role in cancer as a tumor suppressor. KLF10 demonstrate anti-proliferative effects and induce apoptosis in various carcinoma cells including pancreatic cancer, leukemia, and osteoporosis. Collectively, these data indicate that KLF10 plays a significant role in various biological processes and diseases, but its role in cancer is still unclear. Therefore, this review was conducted to describe and discuss the role and function of KLF10 in diseases, including cancer, with a special emphasis on its signaling with TGF-β.
Highlights
Krüppel-like factor 10 (KLF10), originally named TGF-β (Transforming growth factor beta) inducible early gene 1 (TIEG1), is a DNA-binding transcriptional regulator containing a triple C2H2 zinc finger domain
KLF10 is regulated by other members of the TGF-β superfamily, such as bone morphogenetic protein (BMP), activins and GDNF, which suggests that KLF10 might act in diverse signaling pathways at the transcriptional level
Many studies have shown that KLF10 acts as a tumor suppressor through TGF-β signaling by playing an important role in inhibition of cell proliferation and induction of apoptosis (Figure 2) [30,69]
Summary
Transforming growth factor (TGFβ) beta-like group proteins consist of a large family of related. TGFβ superfamily members regulate fundamental cell processes such as proteins are differentiation, the major intracellular mediators oforganization, TGFβ signaling pathway to migration. Smad proteins their target genes [27]. The KLF10 N-terminal protein segments contain three unique repression domains, R1, R2, and were originally as TGF-β early transcriptional gene 1 (TIEG1)factor in human osteoblast (OB). KLF10 is involved in several different types of gene expression in various cell types and serves as a target gene for many signaling pathways This gene is known to be induced by estrogen, TGF-βs, bone morphogenetic protein (BMP), nerve growth factor and epidermal growth factor (EGF) depending on cellular and environmental circumstances. KLF10 is regulated by other members of the TGF-β superfamily, such as BMPs, activins and GDNF (glial cell derived neurotrophic factor), which suggests that KLF10 might act in diverse signaling pathways at the transcriptional level
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