Reduced RECK levels accelerate skeletal muscle differentiation, improve muscle regeneration, and decrease fibrosis

Gutiérrez, Jaime; Gonzalez, David J.; Escalona-Rivano, Rodrigo; Takahashi, Chiaki; Brandan, Enrique

doi:10.1096/fj.202001646rr

Cited by 5 publications

(5 citation statements)

References 112 publications

(284 reference statements)

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“…In hepatocellular carcinoma, RECK expression is associated with less vascular invasion, as well as immunogenic features such as recruitment of tumor-infiltrating lymphocytes and expression of immune checkpoint molecules, including programmed cell death ligand 1 (PD-L1) [64]. In the muscle regeneration process, it has been reported that notch-1 signaling is reduced, while p38 and AKT signaling are augmented in myoblasts with decreased RECK expression levels [65]. Our understanding of the RECK molecular regulation mechanism mediating miR-21 microRNA function in cancer generally and the cervical carcinogenesis process specifically remains limited.…”

Section: Discussionmentioning

confidence: 99%

Mir-21 Regulates Growth and Migration of Cervical Cancer Cells by RECK Signaling Pathway

Aguilar-Martínez,

Campos-Viguri,

Medina-García

et al. 2024

Preprint

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Expression of miR-21 has been found to be altered in almost all types of cancers and it has been classified as an oncogenic microRNA. In addition, expression of tumor suppressor gene RECK is associated with miR-21 overexpression in high-grade cervical lesions. In the present study we analyze the role of miR-21 in RECK gene regulation in cervical cancer cells. To identify the downstream cellular target genes of upstream miR-21, we silenced endogenous miR-21 expression using siRNAs. We analyzed the expression of miR-21 and RECK, as well as functional effects on cell proliferation and migration. We found that in cervical cancer cells there was an inverse correlation between miR-21 expression and RECK mRNA and protein expression. SiRNAs to miR-21 increased luciferase reporter activity in construct plasmids containing the RECK-3′-UTR microRNA response elements MRE21-1, MRE21-2, and MRE21-3. The role of miR-21 in cell proliferation was also analyzed and cancer cells transfected with siRNAs exhibited a markedly reduced cell proliferation and migration. Our findings indicate that miR-21 post-transcriptionally down-regulates the expression of RECK to promote cell proliferation and cell migration inhibition in cervical cancer cell survival. Therefore, miR-21 and RECK may be potential therapeutic targets in gene therapy for cervical cancer.

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Section: Discussionmentioning

confidence: 99%

Mir-21 Regulates Growth and Migration of Cervical Cancer Cells by RECK Signaling Pathway

Aguilar-Martínez,

Campos-Viguri,

Medina-García

et al. 2024

Preprint

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“…In hepatocellular carcinoma, RECK expression is associated with less vascular invasion, as well as PD-L1 expression [68]. In the muscle regeneration process, it has been reported that notch-1 signaling is reduced, while p38 and AKT signaling are augmented in myoblasts with decreased RECK expression levels [69]. Our understanding of the RECK molecular regulation mechanism mediating miR-21 microRNA function in cancer generally and the cervical carcinogenesis process specifically remains limited.…”

Section: Discussionmentioning

confidence: 99%

MiR-21 Regulates Growth and Migration of Cervical Cancer Cells by RECK Signaling Pathway

Aguilar-Martínez,

Campos-Viguri,

Medina-García

et al. 2024

IJMS

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Expression of miR-21 has been found to be altered in almost all types of cancers, and it has been classified as an oncogenic microRNA. In addition, the expression of tumor suppressor gene RECK is associated with miR-21 overexpression in high-grade cervical lesions. In the present study, we analyze the role of miR-21 in RECK gene regulation in cervical cancer cells. To identify the downstream cellular target genes of upstream miR-21, we silenced endogenous miR-21 expression using siRNAs. We analyzed the expression of miR-21 and RECK, as well as functional effects on cell proliferation and migration. We found that in cervical cancer cells, there was an inverse correlation between miR-21 expression and RECK mRNA and protein expression. SiRNAs to miR-21 increased luciferase reporter activity in construct plasmids containing the RECK-3′-UTR microRNA response elements MRE21-1, MRE21-2, and MRE21-3. The role of miR-21 in cell proliferation was also analyzed, and cancer cells transfected with siRNAs exhibited a markedly reduced cell proliferation and migration. Our findings indicate that miR-21 post-transcriptionally down-regulates the expression of RECK to promote cell proliferation and cell migration inhibition in cervical cancer cell survival. Therefore, miR-21 and RECK may be potential therapeutic targets in gene therapy for cervical cancer.

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“…Reversion-inducing-cysteine-rich protein with kazal motifs (RECK) is a membrane-anchored protein that negatively regulates the activity of different MMPs. RECK’s role in skeletal muscle differentiation, regeneration, and fibrosis have only recently been explored, but one study showed that, during myogenic differentiation of C2C12 myoblasts and satellite cells on isolated muscle fibers, RECK was transiently upregulated, and upregulation alternated with periods of RECK reduction [ 42 ]. Additionally, when RECK levels were reduced, C2C12 myoblasts were likely to enter their differentiation program with an accelerated differentiation process.…”

Section: Survey Of Engineered Cell–ecm–materials Interactions In Musc...mentioning

confidence: 99%

“…In vivo results indicated that the transient upregulation of RECK occurs during skeletal muscle regeneration and is accelerated in RECK± mice. The RECK± mice had diminished fibrosis in response to chronic muscle damage compared to WT controls, suggesting that RECK acts as a myogenic repressor during muscle formation and regeneration [ 42 ]. Attenuating the effects of RECK in the ECM may prove useful for engineered and regenerative muscle therapies.…”

Section: Survey Of Engineered Cell–ecm–materials Interactions In Musc...mentioning

confidence: 99%

Engineering Cell–ECM–Material Interactions for Musculoskeletal Regeneration

2023

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The extracellular microenvironment regulates many of the mechanical and biochemical cues that direct musculoskeletal development and are involved in musculoskeletal disease. The extracellular matrix (ECM) is a main component of this microenvironment. Tissue engineered approaches towards regenerating muscle, cartilage, tendon, and bone target the ECM because it supplies critical signals for regenerating musculoskeletal tissues. Engineered ECM–material scaffolds that mimic key mechanical and biochemical components of the ECM are of particular interest in musculoskeletal tissue engineering. Such materials are biocompatible, can be fabricated to have desirable mechanical and biochemical properties, and can be further chemically or genetically modified to support cell differentiation or halt degenerative disease progression. In this review, we survey how engineered approaches using natural and ECM-derived materials and scaffold systems can harness the unique characteristics of the ECM to support musculoskeletal tissue regeneration, with a focus on skeletal muscle, cartilage, tendon, and bone. We summarize the strengths of current approaches and look towards a future of materials and culture systems with engineered and highly tailored cell–ECM–material interactions to drive musculoskeletal tissue restoration. The works highlighted in this review strongly support the continued exploration of ECM and other engineered materials as tools to control cell fate and make large-scale musculoskeletal regeneration a reality.

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Reduced RECK levels accelerate skeletal muscle differentiation, improve muscle regeneration, and decrease fibrosis

Cited by 5 publications

References 112 publications

Mir-21 Regulates Growth and Migration of Cervical Cancer Cells by RECK Signaling Pathway

Mir-21 Regulates Growth and Migration of Cervical Cancer Cells by RECK Signaling Pathway

MiR-21 Regulates Growth and Migration of Cervical Cancer Cells by RECK Signaling Pathway

Engineering Cell–ECM–Material Interactions for Musculoskeletal Regeneration

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