SMARCC2 combined with c‑Myc inhibits the migration and invasion of glioma cells via modulation of the Wnt/β‑catenin signaling pathway

Li, Chiyang; Fei, Chengshuo; Li, Junjie; Wu, Hang; Chen, Lei; Roshani, Ramzi; Li, Hong; Shi, Linyong; Gu, Junwei; Lu, Yuntao; Zhou, Qiang

doi:10.3892/mmr.2021.12190

Cited by 9 publications

(4 citation statements)

References 41 publications

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“…These data are in line with the findings that HOTAIR regulated genes were enriched in the pathways “actin cytoskeleton” and “Wnt signaling” (Supplementary Data 3 and Fig. 5a ), which were previously linked to tissue remodelling and cell migration 44 , 45 . Furthermore, HOTAIR silencing increased Fas-induced apoptosis in SF (Fig.…”

Section: Resultssupporting

confidence: 91%

The long non-coding RNA HOTAIR contributes to joint-specific gene expression in rheumatoid arthritis

Elhai,

Micheroli,

Houtman

et al. 2023

Nat Commun

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Although patients with rheumatoid arthritis (RA) typically exhibit symmetrical joint involvement, some patients develop alternative disease patterns in response to treatment, suggesting that different molecular mechanism may underlie disease progression depending on joint location. Here, we identify joint-specific changes in RA synovium and synovial fibroblasts (SF) between knee and hand joints. We show that the long non-coding RNA HOTAIR, which is only expressed in knee SF, regulates more than 50% of this site-specific gene expression in SF. HOTAIR is downregulated after stimulation with pro-inflammatory cytokines and is expressed at lower levels in knee samples from patients with RA, compared with osteoarthritis. Knockdown of HOTAIR in knee SF increases PI-Akt signalling and IL-6 production, but reduces Wnt signalling. Silencing HOTAIR inhibits the migratory function of SF, decreases SF-mediated osteoclastogenesis, and increases the recruitment of B cells by SF. We propose that HOTAIR is an important epigenetic factor in joint-specific gene expression in RA.

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Section: Resultssupporting

confidence: 91%

The long non-coding RNA HOTAIR contributes to joint-specific gene expression in rheumatoid arthritis

Elhai,

Micheroli,

Houtman

et al. 2023

Nat Commun

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show abstract

“…These data are in line with the findings that HOTAIR regulated genes were enriched in the pathways "actin cytoskeleton" and "Wnt signaling" (Table S3 and Figure 4G/H), which were previously linked to tissue remodelling and cell migration (39,40).…”

Section: Hotair Downregulation Alters Key Functions In Sf and Surroun...supporting

confidence: 90%

The long-non coding RNA HOTAIR as site specific regulator of inflammation in chronic arthritis

Elhaï¹,

Micheroli

Houtman

et al. 2023

Preprint

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Most forms of arthritis, have a distinctive topographical pattern of joint involvement. Beyond these differences among diseases, there are also differences in phenotype and response to treatment between joints of the same type of arthritis, suggesting that molecular mechanisms may differ depending on joint location. Here we show that there are joint-specific molecular and tissue changes in the synovium and in local stromal cells (synovial fibroblasts;SF). The long non-coding RNA HOTAIR, expressed only in lower extremities SF, regulates much of this site-specific gene expression in SF. Downregulation of HOTAIR after TNF stimulation regulated relevant inflammatory pathways by epigenetic and transcriptional mechanisms and modified the migratory function of SF, decreased SF-mediated osteoclastogenesis, and increased the attraction of B cells by SF. Since site-specific expression of HOTAIR was also measured in the skin, spine and gastrointestinal tract, we propose HOTAIR as important epigenetic factor that modulates site-specific phenotypes of chronic inflammation.

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“…Previous research has extensively expounded on Wnt-mediated signaling pathways and their in uence on embryonic development, tissue homeostasis, and tumorigenesis [31]. In this respect, SMARCC2 has been implicated in mediating the Wnt/β-catenin signaling pathway to suppress glioma cell migration and invasion through interaction with C-MYC [32]. Our KEGG pathway analysis consistently highlighted the signi cant role of the Wnt signaling pathway in TRIM37-mediated signaling transduction.…”

Section: Discussionmentioning

confidence: 53%

N6-methyladenosine-modified TRIM37 augments sunitinib resistance by promoting the ubiquitin-degradation of SmARCC2 via activating the Wnt signaling pathway in renal cell carcinoma

Luo,

Dai,

Dong

et al. 2023

Preprint

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Tripartite motif-containing 37 (TRIM37) is reportedly a key member of the superfamily of TRIM proteins. Emerging evidence underscores the close association between dysregulated TRIM37 expression and the progression of various human malignancies. However, the precise biological functions and regulatory mechanisms of TRIM37 remain elusive. This study aimed to elucidate the impact of TRIM37 on the chemotherapy sensitivity of renal cell carcinoma (RCC) and uncover its specific molecular regulatory role. Using RT-qPCR and western blot assays, we assessed TRIM37 expression in both RCC patients and RCC cells. Through in vitro and in vivo experiments, we investigated the effects of TRIM37 silencing and overexpression on RCC cell proliferation, stemness capacity, and chemotherapy sensitivity using colony formation and sphere formation assays. Additionally, a co-immunoprecipitation (Co-IP) experiment was conducted to explore putative interacting proteins. Our results revealed elevated TRIM37 expression in both RCC patient tumor tissues and RCC cells. Functional experiments consistently demonstrated that TRIM37 silencing reduced proliferation and stemness capacity while enhancing chemotherapy sensitivity in RCC cells. Furthermore, we discovered that TRIM37 mediates the degradation of SMARCC2 via ubiquitin-proteasome pathways by activating the Wnt signaling pathway. In conclusion, this study not only sheds light on the biological role of TRIM37 in RCC progression but also identifies a potential molecular target for therapeutic intervention in RCC patients.

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SMARCC2 combined with c‑Myc inhibits the migration and invasion of glioma cells via modulation of the Wnt/β‑catenin signaling pathway

Cited by 9 publications

References 41 publications

The long non-coding RNA HOTAIR contributes to joint-specific gene expression in rheumatoid arthritis

The long non-coding RNA HOTAIR contributes to joint-specific gene expression in rheumatoid arthritis

The long-non coding RNA HOTAIR as site specific regulator of inflammation in chronic arthritis

N6-methyladenosine-modified TRIM37 augments sunitinib resistance by promoting the ubiquitin-degradation of SmARCC2 via activating the Wnt signaling pathway in renal cell carcinoma

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