Transcription Factor KLF7 Promotes Osteoclast Differentiation by Suppressing HO-1

Chen, Changhong; Hu, Fei; Miao, Shichang; Sun, Liping; Jiao, Ya-Jun; Xu, Min; Huang, Xin; Ying, Yang; Zhou, Rong-Fu

doi:10.3389/fgene.2022.798433

Cited by 10 publications

(9 citation statements)

References 29 publications

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“…have discovered that KLF7 can affect the bone mineral density (BMD) of patients through sequencing and bioinformatics, which seems to make it possible that KLF7 will be a target for the treatment of OP 193 . A study in 2022 showed that KLF7 was low expressed in people with high BMD, and KLF7 was an upstream regulator of HO‐1 194 . Knockdown of KLF7 impaired osteoclast differentiation, whereas high expression of KLF7 markedly reduced the expression of HO‐1, a negative regulator of osteoclast differentiation, and increased the expression levels of osteoclast marker proteins (TRAP, NFAT2 and CTSK) 194,195 .…”

Section: Role Of Klfs In Bone Diseasesmentioning

confidence: 99%

“…A study in 2022 showed that KLF7 was low expressed in people with high BMD, and KLF7 was an upstream regulator of HO‐1 194 . Knockdown of KLF7 impaired osteoclast differentiation, whereas high expression of KLF7 markedly reduced the expression of HO‐1, a negative regulator of osteoclast differentiation, and increased the expression levels of osteoclast marker proteins (TRAP, NFAT2 and CTSK) 194,195 . In short, KLF7 promotes osteoclast differentiation by negatively regulating the expression of HO‐1, thus aggravating OP.…”

Section: Role Of Klfs In Bone Diseasesmentioning

confidence: 99%

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KLF transcription factors in bone diseases

Wang,

Han,

Dmitrii

et al. 2024

J Cellular Molecular Medi

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Krüppel‐like factors (KLFs) are crucial in the development of bone disease. They are a family of zinc finger transcription factors that are unusual in containing three highly conserved zinc finger structural domains interacting with DNA. It has been discovered that it engages in various cell functions, including proliferation, apoptosis, autophagy, stemness, invasion and migration, and is crucial for the development of human tissues. In recent years, the role of KLFs in bone physiology and pathology has received adequate attention. In addition to regulating the normal growth and development of the musculoskeletal system, KLFs participate in the pathological process of the bones and joints and are intimately linked to several skeletal illnesses, such as osteoarthritis (OA), rheumatoid arthritis (RA), osteoporosis (OP) and osteosarcoma (OS). Consequently, targeting KLFs has emerged as a promising therapeutic approach for an array of bone disorders. In this review, we summarize the current literature on the importance of KLFs in the emergence and regulation of bone illnesses, with a particular emphasis on the pertinent mechanisms by which KLFs regulate skeletal diseases. We also discuss the need for KLFs‐based medication‐targeted treatment. These endeavours offer new perspectives on the use of KLFs in bone disorders and provide prognostic biomarkers, therapeutic targets and possible drug candidates for bone diseases.

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Section: Role Of Klfs In Bone Diseasesmentioning

confidence: 99%

Section: Role Of Klfs In Bone Diseasesmentioning

confidence: 99%

KLF transcription factors in bone diseases

Wang,

Han,

Dmitrii

et al. 2024

J Cellular Molecular Medi

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“…Leading edge genes revealed in GSEA enrichment of "connective tissue development" (Figure 2D) included SOX9, a key developmental TF which has been implicated in fibroblast activation and fibrosis 23 , KLF7 a TF involved in osteoclast differentiation 24 and has been implicated in cancers [25][26] , HMGA2 which is induced by Fibroblast Growth Factor 2 and is therefore associated with fibroblast activation 27 , and has been reported to be an independent stromal marker for pancreatic adenocarcinoma. In addition to the gene ontologies associated with wound healing response and fibroblast activation, we also found that hypoxia resulted in enrichment of actin cytoskeletal reorganization.…”

Section: Hypoxia Upregulates Genes Associated With Actomyosin Transfo...mentioning

confidence: 99%

Stable and Oscillatory Hypoxia Differentially Regulate Invasibility of Breast Cancer Associated Fibroblasts

Du,

Novin,

Liu

et al. 2024

Preprint

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As local regions in the tumor outstrip their oxygen supply, hypoxia can develop, affecting not only the cancer cells, but also other cells in the microenvironment, including cancer associated fibroblasts (CAFs). Hypoxia is also not necessarily stable over time, and can fluctuate or oscillate. Hypoxia Inducible Factor-1 is the master regulator of cellular response to hypoxia, and can also exhibit oscillations in its activity. To understand how stable, and fluctuating hypoxia influence breast CAFs, we measured changes in gene expression in CAFs in normoxia, hypoxia, and oscillatory hypoxia, as well as measured change in their capacity to resist, or assist breast cancer invasion. We show that hypoxia has a profound effect on breast CAFs causing activation of key pathways associated with fibroblast activation, but reduce myofibroblast activation and traction force generation. We also found that oscillatory hypoxia, while expectedly resulted in a sub-hypoxic response in gene expression, it resulted in specific activation of pathways associated with actin polymerization and actomyosin maturation. Using traction force microscopy, and a nanopatterned stromal invasion assay, we show that oscillatory hypoxia increases contractile force generation vs stable hypoxia, and increases heterogeneity in force generation response, while also additively enhancing invasibility of CAFs to MDA-MB-231 invasion. Our data show that stable and unstable hypoxia can regulate many mechnobiological characteristics of CAFs, and can contribute to transformation of CAFs to assist cancer dissemination and onset of metastasis.

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“…It has been reported that KLF7 is lowly expressed in people with high bone mineral density [ 81 ]. By comparing the gene expression profiles of normal and aged senescent human osteoblasts, Chen et al identified miRNA targeting KLF7 as one of the genes significantly upregulated in aged osteoblasts [ 82 ].…”

Section: Roles Of Klfs In Normal Bone Physiology ( Table 1 ...mentioning

confidence: 99%

“…In contrast, osteoclast differentiation was enhanced by KLF7. Mechanistically, KLF7 directly represses heme oxygenase-1 (HO-1) expression, which is known as a negative regulator of osteoclast differentiation [ 81 , 83 , 84 , 85 ].…”

Section: Roles Of Klfs In Normal Bone Physiology ( Table 1 ...mentioning

confidence: 99%

Kruppel-like Factors in Skeletal Physiology and Pathologies

Abe

Saeki

Ikeda

et al. 2022

IJMS

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Kruppel-like factors (KLFs) belong to a large group of zinc finger-containing transcription factors with amino acid sequences resembling the Drosophila gap gene Krüppel. Since the first report of molecular cloning of the KLF family gene, the number of KLFs has increased rapidly. Currently, 17 murine and human KLFs are known to play crucial roles in the regulation of transcription, cell proliferation, cellular differentiation, stem cell maintenance, and tissue and organ pathogenesis. Recent evidence has shown that many KLF family molecules affect skeletal cells and regulate their differentiation and function. This review summarizes the current understanding of the unique roles of each KLF in skeletal cells during normal development and skeletal pathologies.

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Transcription Factor KLF7 Promotes Osteoclast Differentiation by Suppressing HO-1

Cited by 10 publications

References 29 publications

KLF transcription factors in bone diseases

KLF transcription factors in bone diseases

Stable and Oscillatory Hypoxia Differentially Regulate Invasibility of Breast Cancer Associated Fibroblasts

Kruppel-like Factors in Skeletal Physiology and Pathologies

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