MicroRNA-21 Affects Proliferation and Apoptosis by Regulating Expression of PTEN in Human Keloid Fibroblasts

Liu, Ying; Wang, Xiaoxue; Yang, Dae Suk; Xiao, Zhibo; Chen, Xi

doi:10.1097/prs.0000000000000577

Cited by 60 publications

(53 citation statements)

References 40 publications

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“…As a matter of fact, multiple miRs members, including miR-196, miR-21, and miR-199a-5p, have shown their potential in antagonizing keloids, 15,42,43 but few ones are capable of directly interacting with VEGF in these skin disorders. The theory commonly accepted is that onset of keloids is associated with an abundance of growth factors and cytokines, 44 especially VEGF which favors blood vessels hyperpermeable and continued induction of tissue granulation of the healing wounds.…”

Section: Discussionmentioning

confidence: 99%

RETRACTED: Upregulation of microRNA-205 suppresses vascular endothelial growth factor expression-mediated PI3K/Akt signaling transduction in human keloid fibroblasts

Liang

Sheng

et al. 2016

Exp Biol Med (Maywood)

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Keloid is one of the most frustrating problems related to wounding healing and presents a great challenge in clinic. MicroRNAs (miRs) have shown their potential as a novel therapy for the prevention and treatment of keloid. Vascular endothelial growth factor (VEGF) plays a critical role in the regulation of scar development. In the current study, it was hypothesized that miR-205-5p was capable of suppressing keloid formation by inhibiting the VEGF-mediated wound healing cascade. The expression statuses of miR-205-5p and VEGF in clinical keloid tissues and keloid cell line human keloid fibroblasts (HKF) were detected. Then the direct action of miR-205-5p on VEGF gene was assessed using dual-luciferase assay. Thereafter, orchestrated administrations on HKF with miR-205-5p mimic, specific VEGF siRNA, PI3K agonist (740 Y-P), and PI3K inhibitor (LY294002) were performed to reveal the roles of miR-205-5p and VEGF in keloid formation and further explain the mechanism through which miR-205-5p affected the VEGF-mediated signaling transductions. Our results showed that there was significant low expression of miR-205-5p in keloid tissue specimens and the cell line while the expression of VEGF in keloid tissues was augmented. Moreover, miR-205-5p overexpression dramatically impaired the cell viability, induced the cell apoptosis, and inhibited the cell invasion and migration ability in HKF. Based on the detection of dual luciferase assay and detection at protein level, miR-205-5p antagonized the keloids by directly targeting VEGF expression and subsequently inhibiting PI3K/Akt pathway. The current study is the first one demonstrating that miR-205-5p inhibits the pathogenesis of keloids, indicating the potential of miR-205-5p in the development of therapies for prevention and treatment of keloids.

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Section: Discussionmentioning

confidence: 99%

RETRACTED: Upregulation of microRNA-205 suppresses vascular endothelial growth factor expression-mediated PI3K/Akt signaling transduction in human keloid fibroblasts

Liang

Sheng

et al. 2016

Exp Biol Med (Maywood)

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“…miRNA‐31, with increased expression level in the keloid disease, may contribute to extensive fibroblast proliferation and the deposition of extracellular matrix and collagen in the formation of the keloid . miRNA‐21 was demonstrated to express at significantly higher levels in keloid fibroblasts compared to normal ones, considering its major function in promoting cell proliferation and collagen synthesis via targeting PTEN, Smad7, regulating the ratio of BAX to BCL‐2 . miRNA‐29a was recognized as a crucial therapeutic target for fibrosis diseases.…”

Section: Discussionmentioning

confidence: 99%

Identification and integrated analysis of microRNA expression profiles in keloid

Zhong

Bian

Lyu

et al. 2018

J of Cosmetic Dermatology

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“…176,177 Several putative regulators of PTEN have been reported, including caveolin-1, 178,179 DJ-1, 180 and miR-21. [181][182][183][184][185][186][187][188] Remarkably, lower expression of caveolin-1 has been reported in adenomyosis, 189 and higher expression of DJ-1 153,190 and miR-21 191,192 has been reported in endometriosis as well. Inactivation of FOXO3a by SGK1 and ERβ also has been reported in endometriosis.…”

Section: Ptenmentioning

confidence: 98%

“…Aberrant PTEN/AKT signaling inactivates FOXO3a, a proapoptotic factor, promoting fibrosis . Several putative regulators of PTEN have been reported, including caveolin‐1, DJ‐1, and miR‐21 . Remarkably, lower expression of caveolin‐1 has been reported in adenomyosis, and higher expression of DJ‐1 and miR‐21 has been reported in endometriosis as well.…”

Section: Mutations Of Cancer Driver Genes In Endometriosis and Their mentioning

confidence: 99%

Cancer driver mutations in endometriosis: Variations on the major theme of fibrogenesis

Guo

2018

Reprod Medicine & Biology

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BackgroundOne recent study reports cancer driver mutations in deep endometriosis, but its biological/clinical significance remains unclear. Since the natural history of endometriosis is essentially gradual progression toward fibrosis, it is thus hypothesized that the six driver genes reported to be mutated in endometriosis (the RP set) may play important roles in fibrogenesis but not necessarily malignant transformation.MethodsExtensive PubMed search to see whether RP and another set of driver genes not yet reported (NR) to be mutated in endometriosis have any roles in fibrogenesis. All studies reporting on the role of fibrogenesis of the genes in both RP and NR sets were retrieved and evaluated in this review.ResultsAll six RP genes were involved in various aspects of fibrogenesis as compared with only three NR genes. These nine genes can be anchored in networks linking with their upstream and downstream genes that are known to be aberrantly expressed in endometriosis, piecing together seemingly unrelated findings.ConclusionsGiven that somatic driver mutations can and do occur frequently in physiologically normal tissues, it is argued that these mutations in endometriosis are not necessarily synonymous with malignancy or premalignancy, but the result of enormous pressure for fibrogenesis.

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MicroRNA-21 Affects Proliferation and Apoptosis by Regulating Expression of PTEN in Human Keloid Fibroblasts

Abstract: This in vitro study demonstrates important interactions among miR-21 expression, keloid fibroblast apoptosis, cell proliferation, and some related proteins. These findings may provide some hints toward effective applications of miR-21 as a therapy target for keloids.

Cited by 60 publications

References 40 publications

RETRACTED: Upregulation of microRNA-205 suppresses vascular endothelial growth factor expression-mediated PI3K/Akt signaling transduction in human keloid fibroblasts

RETRACTED: Upregulation of microRNA-205 suppresses vascular endothelial growth factor expression-mediated PI3K/Akt signaling transduction in human keloid fibroblasts

Identification and integrated analysis of microRNA expression profiles in keloid

Cancer driver mutations in endometriosis: Variations on the major theme of fibrogenesis

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