LncRNA GNAS-AS1 knockdown inhibits keloid cells growth by mediating the miR-188-5p/RUNX2 axis

Liu, Yun; Li, Lei; Wang, Jia-Yao; Gao, Fei; Lin, Xia; Lin, Shi-Shuai; Qiu, Zhi-Yang; Liang, Zun‐Hong

doi:10.1007/s11010-022-04538-6

Cited by 3 publications

(6 citation statements)

References 47 publications

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“…Liu et al. reported enhanced GNAS‐AS1 expression in clinical keloid tissues and HKFs and that GNAS‐AS1 silencing attenuated the proliferation, migration, and invasion capabilities of HKFs by regulating the miR‐188‐5p/RUNX2 axis 9 . Similarly, our experimental results also confirmed that GNAS‐AS1 expression was abnormally high in clinical keloid samples and HKFs and that GNAS‐AS1 knockdown inhibited the proliferation, migration and ECM accumulation of HKFs.…”

Section: Discussionsupporting

confidence: 87%

“…GNAS‐AS1 expression is enhanced in clinical keloid tissues and HKFs and GNAS‐AS1 silencing inhibits keloid progression 9 . Our results validated the abnormally high levels of GNAS‐AS1 expression in clinical keloid tissues compared with tissues from healthy volunteers (Figure 1A).…”

Section: Resultssupporting

confidence: 77%

“…For instance, lncRNA 19, lncRNA ZNF252P‐AS1 and lncRNA HOXA11‐AS were reported as involved in keloid progression through the growth of keloid fibroblasts (KFs) 6–8 . Furthermore, abnormal expression of GNAS antisense RNA 1 (GNAS‐AS1) was observed in clinical keloid tissues and HKFs, and GNAS‐AS1 downregulation attenuated HKF proliferation, migration and invasion 9 . However, the molecular mechanism of GNAS‐AS1 involvement in keloids requires further elucidation.…”

Section: Introductionmentioning

confidence: 99%

“…[6][7][8] Furthermore, abnormal expression of GNAS antisense RNA 1 (GNAS-AS1) was observed in clinical keloid tissues and HKFs, and GNAS-AS1 downregulation attenuated HKF proliferation, migration and invasion. 9 However, the molecular mechanism of GNAS-AS1 involvement in keloids requires further elucidation.…”

Section: Introductionmentioning

confidence: 99%

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STAT3‐induced lncRNA GNAS‐AS1 accelerates keloid formation by mediating the miR‐196a‐5p/CXCL12/STAT3 axis in a feedback loop

Liu,

Ma,

Fan

et al. 2024

Experimental Dermatology

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Keloids are pathological scar tissue resulting from skin trauma or spontaneous formation, often accompanied by itching and pain. Although GNAS antisense RNA 1 (GNAS‐AS1) shows abnormal upregulation in keloids, the underlying molecular mechanism is unclear. The levels of genes and proteins in clinical tissues from patients with keloids and human keloid fibroblasts (HKFs) were measured using quantitative reverse transcription PCR, western blot and enzyme‐linked immunosorbent assay. The features of HKFs, including proliferation and migration, were evaluated using cell counting kit 8 and a wound healing assay. The colocalization of GNAS‐AS1 and miR‐196a‐5p in HKFs was measured using fluorescence in situ hybridization. The relationships among GNAS‐AS1, miR‐196a‐5p and C‐X‐C motif chemokine ligand 12 (CXCL12) in samples from patients with keloids were analysed by Pearson correlation analysis. Gene interactions were validated by chromatin immunoprecipitation and luciferase reporter assays. GNAS‐AS1 and CXCL12 expression were upregulated and miR‐196a‐5p expression was downregulated in clinical tissues from patients with keloids. GNAS‐AS1 knockdown inhibited proliferation, migration, and extracellular matrix (ECM) accumulation of HKFs, all of which were reversed by miR‐196a‐5p downregulation. Signal transducer and activator of transcription 3 (STAT3) induced GNAS‐AS1 transcription through GNAS‐AS1 promoter interaction, and niclosamide, a STAT3 inhibitor, decreased GNAS‐AS1 expression. GNAS‐AS1 positively regulated CXCL12 by sponging miR‐196‐5p. Furthermore, CXCL12 knockdown restrained STAT3 phosphorylation in HKFs. Our findings revealed a feedback loop of STAT3/GNAS‐AS1/miR‐196a‐5p/CXCL12/STAT3 that promoted HKF proliferation, migration and ECM accumulation and affected keloid progression.

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Section: Discussionsupporting

confidence: 87%

Section: Resultssupporting

confidence: 77%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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STAT3‐induced lncRNA GNAS‐AS1 accelerates keloid formation by mediating the miR‐196a‐5p/CXCL12/STAT3 axis in a feedback loop

Liu,

Ma,

Fan

et al. 2024

Experimental Dermatology

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“…CCK-8 assay was performed as previously described. 35 Briefly, HKFs in each group were incubated at 37°C for 24, 48, and 72 h, followed by the addition of CCK-8 reagent (Dojindo Molecular Technologies, Kumamoto, Japan) (10 μL/well) at each time point and 2-h incubation at 37°C with 5% CO 2 . A microplate reader (Tecan Group, Switzerland) was employed to detect absorbance at 450 nm.…”

Section: Cck-8 Assaymentioning

confidence: 99%

Effects of extracellular vesicles from adipose‐derived stem cells on human keloid fibroblasts via the SOCS1/JAK2/STAT3 pathway

Ruan,

Wang,

Shi

et al. 2024

J of Cosmetic Dermatology

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BackgroundKeloid represents a benign skin tumor with many cancer‐like features. Extracellular vesicles (EVs) derived from human adipose‐derived stem cells (hADSCs) play a role in cell migration of multiple diseases.AimsThis study aimed to investigate the impact of hADSC‐EVs on human keloid fibroblasts (HKFs).MethodshADSCs were cultured to the 3rd generation, and subsequently assessed for their osteogenic, adipogenic, and chondrogenic differentiative abilities using flow cytometry, alizarin red, oil red O, and alcian blue staining techniques. hADSC‐EVs were isolated through ultracentrifugation and subsequently identified. HKFs at the 3rd generation were subjected to treatment with hADSC‐EVs to observe their endocytosis of EVs by immunofluorescence. CCK‐8, wound healing, and Transwell assays were performed to test HKF proliferation and migration. The levels of autophagy proteins, collagens, and Janus kinase 2 (JAK2) and Signal Transducer and Activator of Transcription 3 (STAT3) were determined through Western blot analysis. Suppressor of cytokine signaling 1 (SOCS1) expression was determined by RT‐qPCR and Western blot.ResultshADSC‐EVs were successfully isolated from hADSCs. PKH67‐labeled hADSC‐EVs were observed to be endocytosed by HKFs, resulting the inhibition of HKF proliferation, migration, as well as a reduction in collagen deposition. hADSC‐EVs carried SOCS1 into HKFs to suppress HKF autophagy. SOCS1 downregulation in hADSC‐EVs partially nullified the inhibitory effect of hADSC‐EVs on HKFs. hADSC‐EV‐carried SOCS1 inhibited the activation of the JAK2/STAT3 pathway. JAK2/STAT3 pathway activation partially abrogated the suppression of hADSC‐EVs on the proliferation, migration, and collagen deposition of HKF.ConclusionhADSC‐EVs carried SOCS1 into HKFs and suppressed HKF autophagy, proliferation, migration, and collagen deposition by inactivating the JAK2/STAT3 pathway.

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Non-coding RNAs in hypertrophic scars and keloids: Current research and clinical relevance: A review

Su,

Han

2024

International Journal of Biological Macromolecules

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LncRNA GNAS-AS1 knockdown inhibits keloid cells growth by mediating the miR-188-5p/RUNX2 axis

Cited by 3 publications

References 47 publications

STAT3‐induced lncRNA GNAS‐AS1 accelerates keloid formation by mediating the miR‐196a‐5p/CXCL12/STAT3 axis in a feedback loop

STAT3‐induced lncRNA GNAS‐AS1 accelerates keloid formation by mediating the miR‐196a‐5p/CXCL12/STAT3 axis in a feedback loop

Effects of extracellular vesicles from adipose‐derived stem cells on human keloid fibroblasts via the SOCS1/JAK2/STAT3 pathway

Non-coding RNAs in hypertrophic scars and keloids: Current research and clinical relevance: A review

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