Roquin2 suppresses breast cancer progression by inhibiting tumor angiogenesis via selectively destabilizing proangiogenic factors mRNA

Zhou, Meicen; Lu, Wenbao; Li, Bingwei; Yuan, Xiaochen; Liu, Mingming; Han, Jiahong; Liu, Xueting; Li, Ailing

doi:10.7150/ijbs.59891

Cited by 9 publications

(4 citation statements)

References 37 publications

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“…Interestingly, when subdividing the control group into subgroups according to the origin of the renal biopsies, our IHC results showed a high expression of Regnase-1 and Roquins especially in non-malignant regions of the biopsies taken from nephrectomy specimens, unlike autopsy biopsies. This observation suggests the involvement of these RBPs in renal cancer pathology as supported by other studies, which revealed an important role of Regnase-1 in the regulation of angiogenesis and metastasis of renal cell carcinomas [ 30 ], and have involved the Roquins role in tumor suppression [ 31 , 32 ]. On the other hand, Pospiech et al hypothesized that variation in ZC3H12A may be associated with the risk of clear cell renal cell carcinoma development [ 30 ].…”

Section: Discussionsupporting

confidence: 71%

Differential Expression of Anti-Inflammatory RNA Binding Proteins in Lupus Nephritis

Fakhfakh

Bouallegui

Houssaini

et al. 2022

Life

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Lupus nephritis (LN) is a type of immunological complex glomerulonephritis characterized by chronic renal inflammation which is exacerbated by infiltrating leukocytes and fueled by a variety of pro-inflammatory cytokines. A profound understanding of the pathogenesis of LN is necessary to identify the optimal molecular targets. The role of RNA-binding proteins (RBPs) in post-transcriptional gene regulation in the immune system is being explored in greater depth to better understand how this regulation is implicated in inflammatory and autoimmune diseases. Tristetraprolin (TTP), Roquin-1/2, and Regnase-1 are 3 RBPs that play a critical role in the regulation of pro-inflammatory mediators by gating the degradation and/or translational silencing of target mRNAs. In this study, we proposed to focus on the differential expression of these RBPs in immune cells and renal biopsies from LN patients, as well as their regulatory impact on a specific target. Herein, we highlight a novel target of anti-inflammatory treatment by revealing the mechanisms underlying RBP expression and the interaction between RBPs and their target RNAs.

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Section: Discussionsupporting

confidence: 71%

Differential Expression of Anti-Inflammatory RNA Binding Proteins in Lupus Nephritis

Fakhfakh

Bouallegui

Houssaini

et al. 2022

Life

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“…EDN1 has been shown to be overexpressed in a variety of solid tumors [ 30 – 33 ]. Endothelins (EDNS) had three subtypes: EDN1, EDN2, and EDN3.…”

Section: Discussionmentioning

confidence: 99%

ARHGEF2/EDN1 pathway participates in ER stress-related drug resistance of hepatocellular carcinoma by promoting angiogenesis and malignant proliferation

et al. 2022

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Endoplasmic reticulum (ER) stress is widely involved in the drug resistance of hepatocellular carcinoma (HCC), but the mechanism of ER stress-induced drug resistance involves multiple signaling pathways that cannot be fully explained. Exploring genes associated with ER stress could yield a novel therapeutic target for ER stress-induced drug resistance. By analyzing RNA-sequencing, ATAC-sequencing, and Chip-sequencing data of Tunicamycin (TM)-treated or untreated HCC cells, we found that Rho guanine nucleotide exchange factor 2 (ARHGEF2) is upregulated in HCC cells with ER stress. ARHGEF2 plays an active role in tumor malignant progression. Notwithstanding, no research has been done on the link between ER stress and ARHGEF2. The function of ARHGEF2 as a novel downstream effector of ER stress in the angiogenesis and treatment resistance of HCC was revealed in this work. ARHGEF2 overexpression was linked to malignant development and a poor prognosis in HCC. ER stress stimulates the expression of ARHGEF2 through upregulation of ZNF263. Elevated ARHGEF2 accelerates HCC angiogenesis via the EDN1 pathway, enhances HCC cell proliferation and tumor growth both in vitro and in vivo, and contributes to ER stress-related treatment resistance. HCC cell growth was more inhibited when ARHGEF2 knockdown was paired with targeted medicines. Collectively, we uncovered a previously hidden mechanism where ARHGEF2/EDN1 pathway promotes angiogenesis and participates in ER stress-related drug resistance in HCC.

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“…PDGF promotes angiogenesis by enhancing VEGF and PDGF signaling and VEGF gene expression and activating PDGF receptors (PDGFRs), or by upregulating stromal VEGF [ 12 ]. In particular, PDGF-C is a potent mediator of cell migration, growth, survival, transformation, apoptosis, tissue development, and wound healing; stimulates Ewing’s sarcoma proliferation; and induces paracrine signaling events in whole tumor lysates [ 13 , 14 ]. Moreover, a significant positive correlation exists between PDGFR-α and chondrosarcoma tumor aggressiveness [ 15 ].…”

Section: Introductionmentioning

confidence: 99%

Visfatin-Induced Inhibition of miR-1264 Facilitates PDGF-C Synthesis in Chondrosarcoma Cells and Enhances Endothelial Progenitor Cell Angiogenesis

Song

Chang

Lin

et al. 2022

Cells

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New treatments for chondrosarcoma are extremely important. Chondrosarcoma is a primary malignant bone tumor with a very unfavorable prognosis. High-grade chondrosarcoma has a high potential to metastasize to any organ in the body. Platelet-derived growth factor (PDGF) is a potent angiogenic factor that promotes tumor angiogenesis and metastasis. The adipocytokine visfatin promotes metastatic potential of chondrosarcoma; however, the role of visfatin in angiogenesis in human chondrosarcoma is unclear. We report that the levels of PDGF-C expression were positively correlated with tumor stages, significantly higher than the levels of expression in normal cartilage. Visfatin increased PDGF-C expression and endothelial progenitor cell (EPC) angiogenesis through the PI3K/Akt/mTOR signaling pathway, and dose-dependently down-regulated the synthesis of miR-1264, which targets the 3′-UTR of PDGF-C. Additionally, we discovered inhibition of visfatin or PDGF-C in chondrosarcoma tumors significantly reduced tumor angiogenesis and size. Our results indicate that visfatin inhibits miR-1264 production through the PI3K/Akt/mTOR signaling cascade, and thereby promotes PDGF-C expression and chondrosarcoma angiogenesis. Visfatin may be worth targeting in the treatment of chondrosarcoma angiogenesis.

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Roquin2 suppresses breast cancer progression by inhibiting tumor angiogenesis via selectively destabilizing proangiogenic factors mRNA

Cited by 9 publications

References 37 publications

Differential Expression of Anti-Inflammatory RNA Binding Proteins in Lupus Nephritis

Differential Expression of Anti-Inflammatory RNA Binding Proteins in Lupus Nephritis

ARHGEF2/EDN1 pathway participates in ER stress-related drug resistance of hepatocellular carcinoma by promoting angiogenesis and malignant proliferation

Visfatin-Induced Inhibition of miR-1264 Facilitates PDGF-C Synthesis in Chondrosarcoma Cells and Enhances Endothelial Progenitor Cell Angiogenesis

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