circVMA21 combining with TAF15 stabilizes SOCS3 mRNA to relieve septic lung injury through regulating NF-κB activation

Zhu, Zi-Gui; Liao, Gu-Qing; Zhang, Jianxin; He, Cheng-Jian; Ni, Zhi-Chao

doi:10.1016/j.molimm.2022.07.004

Cited by 5 publications

(3 citation statements)

References 31 publications

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“…In this, we pointed out that ADSCs-Exo derived circVMA21 might alleviate sepsis-related AKI. Many past studies have shown that circVMA21 protects against tissue injury, including lung (26), cartilage (27), and kidney (19,20). Here, circVMA21 was confirmed to have higher expression in ADSCs-Exo, and its expression was enhanced by ADSCs-Exo treatment in vitro and in vivo .…”

Section: Discussionmentioning

confidence: 99%

Exosomal circVMA21 derived from adipose-derived stem cells alleviates sepsis-induced acute kidney injury by targeting miR-16-5p

Huang

et al. 2023

Shock

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Background Exosome from adipose-derived stem cells (ADSCs-Exo) has been shown to inhibit the progression of human diseases, including sepsis-related acute kidney injury (AKI). CircVMA21 is considered to be an important regulator for sepsis-related AKI. However, whether ADSCs-Exo affected sepsis-induced AKI by delivering circVMA21 is not clear. Methods ADSCs was identified by alizarin red staining, oil red O staining, and flow cytometry. ADSCs-Exo was authenticated by transmission electron microscopy, nanoparticle tracking analysis, western blot analysis, and immunofluorescence assay. Cell apoptosis was assessed by flow cytometry, and inflammation cytokine levels were determined by ELISA. Lactate production was assessed using Lactate Acid Content Assay Kit. The expression levels of aerobic glycolysis-related markers, circVMA21 and miR-16-5p were evaluated by qRT-PCR. Dual-luciferase reporter assay and RIP assay were employed to detect RNA interaction. Animal experiments were used to evaluate the role of ADSCs-Exo on renal function and cell injury in LPS-induced AKI mice model. Results ADSCs-Exo inhibited LPS-induced HK-2 cell apoptosis, inflammation and aerobic glycolysis. Knockdown of exosomal circVMA21 derived from ADSCs enhanced HK-2 cell injury induced by LPS. In terms of mechanism, circVMA21 could serve as sponge for miR-16-5p. Besides, miR-16-5p inhibitor reversed the promotion effect of Exo-sh-circVMA21 on LPS-induced cell injury. In addition, ADSCs-Exo protected LPS-induced AKI in mice by increasing circVMA21 expression and decreasing miR-16-5p expression. Conclusion Exosomal circVMA21 derived by ADSCs relieved LPS-induced AKI through targeting miR-16-5p, which provided a potential molecular target for treating sepsis-related AKI.

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Section: Discussionmentioning

confidence: 99%

Exosomal circVMA21 derived from adipose-derived stem cells alleviates sepsis-induced acute kidney injury by targeting miR-16-5p

Huang

et al. 2023

Shock

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“…TAF15 has been implicated in multiple cancers, including breast cancer, gastric cancer, colorectal cancer, lung cancer, and myoepithelial tumors [29][30][31][32][33]. It interacts with lncRNAs and circRNAs to stabilize downstream target genes such as SMAD3 and SOCS3 [28,34]. TEAD4 is TEA domain-containing transcription factor, which is frequently overexpressed in diverse cancers, including ovarian, liver, colorectal, and gastric cancers [35][36][37][38].…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA LINC01106 promotes lung adenocarcinoma progression via upregulation of autophagy

SUN,

ZHENG,

CAI

et al. 2025

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Long noncoding RNA, LINC01106 exhibits high expression in lung adenocarcinoma (LUAD) tumor tissues, but its functional role and regulatory mechanism in LUAD cells remain unclear. LINC01106 expression was analyzed in LUAD tissues and its functional impact on LUAD cells was assessed. LUAD cells were silenced with sh-LINC01106 and injected into nude mice to investigate tumor growth. The downstream transcription factors and molecular mechanism were determined using the Human transcription factor database (TFDB) database and Gene Expression Profiling Interactive Analysis (GEPIA) database. Additionally, the impact of linc01106 on autophagy was analyzed by determining the expression of autophagy-related genes (ATGs) in LUAD cells. Our results showed that LINC01106 exhibited upregulation in both LUAD tissues and cell lines. The silencing of LINC01106 demonstrated a suppressive effect on tumorigenesis in a xenograft mouse model of LUAD. Additionally, LINC01106 was found to recruit TATAbinding protein-associated factor 15 (TAF15), an RNA-binding protein, thereby enhancing the mRNA stability of TEA domain transcription factor 4 (TEAD4). In turn, TEAD4 served as a transcription factor that bound to the LINC01106 promoter and regulated its expression. Further assays indicated that LINC01106 promoted autophagy in LUAD cells by upregulating the expression of autophagy-related genes (ATGs). The silencing of LINC01106 in LUAD cells inhibited autophagy, and cell proliferation, and promoted apoptosis, which all were effectively reversed by ATG5 overexpression. Overall, LINC01106, transcriptionally activated by TEAD4, interacts with TAF15 to promote the stability of TEAD4 and upregulates the expression of ATGs, promoting malignancy of LUAD cells.

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“…Accumulating studies have shown that TAF15 is involved in the processes of human cancers, including extraskeletal myxoid sarcomas, leukaemia, human neuroblastoma, and lung squamous cell carcinoma 18 – 21 . In addition, LncRNAs or circRNAs can combine with TAF15 to stabilize downstream target genes such as SMAD3 mRNA, SOCS3 mRNA, and HMGB3 mRNA to facilitate cell proliferation and migration 9 , 15 , 22 . Moreover, lncRNA GAS5 binding to TAF15 could increase HIF1A expression, resulting in promotion of wound healing in diabetic foot ulcers 23 .…”

Section: Introductionmentioning

confidence: 99%

TAF15 promotes cell proliferation, migration and invasion of gastric cancer via activation of the RAF1/MEK/ERK signalling pathway

Guo

et al. 2023

Sci Rep

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TATA-box-binding protein-associated Factor 15 (TAF15), a member of the FUS/EWS/TAF15 (FET) family, contributes to the progression of various tumours. However, the role and molecular mechanism of TAF15 in gastric cancer (GC) progression are still unknown. In this study, we found that TAF15 was significantly upregulated in GC tumour tissues and cell lines. Overexpression of TAF15 was associated with a larger tumour size, high pathologic stage and high T stage of GC. TAF15 knockdown suppressed the proliferation, migration and invasion of GC cells in vitro and inhibited the tumour growth in vivo. Additionally, TAF15 knockdown led to the significant reductions in the phosphorylation levels of RAF1, MEK and ERK1/2, while total RAF1, MEK and ERK1/2 exhibited no significant change in GC cell lines. In summary, TAF15 is overexpressed in GC tumour tissues and cell lines, and promotes cell proliferation, migration and invasion in GC via the RAF1/MEK/ERK signaling pathway, which suggests that TAF15 might be a potential molecular diagnostic marker or therapeutic target for GC.

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circVMA21 combining with TAF15 stabilizes SOCS3 mRNA to relieve septic lung injury through regulating NF-κB activation

Cited by 5 publications

References 31 publications

Exosomal circVMA21 derived from adipose-derived stem cells alleviates sepsis-induced acute kidney injury by targeting miR-16-5p

Exosomal circVMA21 derived from adipose-derived stem cells alleviates sepsis-induced acute kidney injury by targeting miR-16-5p

Long noncoding RNA LINC01106 promotes lung adenocarcinoma progression via upregulation of autophagy

TAF15 promotes cell proliferation, migration and invasion of gastric cancer via activation of the RAF1/MEK/ERK signalling pathway

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