Heterogeneous nuclear ribonucleoprotein M promotes the progression of breast cancer by regulating the axin/β-catenin signaling pathway

Yang, Weiping; Ding, Mingjian; Cui, Guozhong; Yang, Meng; Dai, Dianlu

doi:10.1016/j.biopha.2018.05.014

Cited by 18 publications

(11 citation statements)

References 29 publications

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“…The destruction complex (DC) consisting of Axin1 and APC, β-catenin and two constitutively active serine-threonine kinases (CK1α/δ and GSK3α/β) plays a crucial role in degrading cytoplasmic β-catenin [38–45]. Axin1 is a key component favoring the DC activity and many upstream molecules of Wnt/β-catenin pathway could meditate its activation by targeting Axin1 in tumor cells [46–48]. Similar to these previous studies, in current study we also found that LDLRAD2 could bind to and inhibit Axin1 from binding to cytoplasmic β-catenin, which largely mitigate the degradation of cytoplasmic β-catenin thereby activating Wnt/β-catenin pathway.…”

Section: Discussionmentioning

confidence: 99%

LDLRAD2 overexpression predicts poor prognosis and promotes metastasis by activating Wnt/β-catenin/EMT signaling cascade in gastric cancer

Wei

Zhang

et al. 2019

Aging

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The therapeutic strategies for advanced gastric cancer (GC) remain unsatisfying and limited. Therefore, it is still imperative to fully elucidate the mechanisms underlying GC aggressive progression. The prognostic value and biological functions of low density lipoprotein receptor class A domain containing protein 2 (LDLRAD2) in GC have never been studied yet. We found that LDLRAD2 expression was significantly upregulated in GC and closely correlated with poor prognosis in GC patients. Functionally, LDLRAD2 promoted epithelial-mesenchymal transition, migration and invasion, and metastasis of GC cells. Mechanistically, LDLRAD2 interacted with and inhibited Axin1 from binding to cytoplasmic β-catenin, which facilitated the nuclear translocation of β-catenin, thereby activating Wnt/β-catenin pathway. Inhibition of β-catenin activity markedly abolished LDLRAD2-induced migration, invasion and metastasis. Together, these results suggested that LDLRAD2 contributed to invasion and metastasis of GC through activating Wnt/β-catenin pathway. LDLRAD2/ Wnt/β-catenin axis may be a potential therapeutic target for GC treatment.

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Section: Discussionmentioning

confidence: 99%

LDLRAD2 overexpression predicts poor prognosis and promotes metastasis by activating Wnt/β-catenin/EMT signaling cascade in gastric cancer

Wei

Zhang

et al. 2019

Aging

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“…β-Catenin is a key factor in the Wnt/β-catenin signaling pathway, and the activation of Wnt signaling could lead to the accumulation of β-catenin in the cytoplasm, which promotes the transcription of c-myc [27]. As the cytoplasmic anchor of β-catenin, AXIN could facilitate the accessibility of β-catenin to the cell nucleus and thereby activate downstream targets [28]. erefore, we measured the influence of Miao and DDP on the expression of β-catenin, AXIN, and c-myc both in vivo and in vitro.…”

Section: Discussionmentioning

confidence: 99%

Chinese Herbal Formulas Miao-Yi-Ai-Tang Inhibits the Proliferation and Migration of Lung Cancer Cells through Targetingβ-Catenin/AXIN and Presents Synergistic Effect with Cisplatin Suppressing Lung Cancer

Zhang

Tan

et al. 2020

BioMed Research International

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Objective. Lung cancer is one of the major causes of cancer deaths worldwide, and the five-year survival still remains low despite the improvement of screening, prevention, and treatment methods. Chinese herbal medicines have been widely used for tumor prevention and treatment. Miao-Yi-Ai-Tang (Miao) is a novel herbal formulation and shows a potential anticancer effect. Materials and Methods. Human Small Cell Lung Cancer Cell was used for study in vitro. After treatments by Miao and Cisplatin (DDP), the invasion, migration, proliferation, and apoptosis of cells were detected by transwell, wound healing, CCK-8, and flow cytometry, respectively. The expression of β-catenin, AXIN, and c-myc was detected by qRT-PCR and immunohistochemistry staining. Western blotting was applied for measuring the protein expression of β-catenin. Subcutaneously transplanted tumor model of lung cancer NCI-H446 was established to investigate the influence of Miao on tumor growth. Results. We found that Miao could inhibit invasion, migration, and proliferation and promote apoptosis of human lung cancer cells. Meanwhile, Miao and DDP presented synergy regulating the proliferation and apoptosis of lung cancer cells. The percentage of lung cancer cells in S and G2 stages was increased markedly by Miao. Besides, the expression of c-myc, AXIN, and β-catenin was markedly inhibited by Miao. Tumor growth in vivo was markedly inhibited by Miao. Conclusions. Chinese herbal formulas Miao could suppress lung cancer through targeting the β-catenin/AXIN signaling pathway. Therefore, our findings may provide a novel strategy for the prevention and treatment of lung cancer.

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“…Among these proteins, U2AF2 (U2 Small Nuclear RNA Auxiliary Factor 2) is a central splicing complex member involved in pre-mRNA splicing and 3′-end processing (65) with an impact in the regulation of transcriptome in activated CD4 T lymphocytes (66). Moreover, HNRNPM (Heterogeneous nuclear ribonucleoprotein M), a component of the spliceosome machinery, promotes alternative spicing, cell proliferation and progression of breast cancer (67), while SRRT (Serrate, RNA Effector Molecule) participates to mRNA splicing and primary miRNA processing (68), it is involved in cell cycle progression at S phase, and its genetic deletion resulted in defective hematopoiesis in bone marrow and thymus (69). DDX21 and DDX58, as RNA helicases unwind their RNA substrates, and are involved in multiple biological processes related to RNA metabolism, including viral dsRNA sensing by innate cells, initiation of host antiviral responses and production of proinflammatory cytokines (70).…”

Section: Discussionmentioning

confidence: 99%

New Insights for RANKL as a Proinflammatory Modulator in Modeled Inflammatory Arthritis

et al. 2019

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Receptor activator of nuclear factor-κB ligand (RANKL), a member of the Tumor Necrosis Factor (TNF) superfamily, constitutes the master regulator of osteoclast formation and bone resorption, whereas its involvement in inflammatory diseases remains unclear. Here, we used the human TNF transgenic mouse model of erosive inflammatory arthritis to determine if the progression of inflammation is affected by either genetic inactivation or overexpression of RANKL in transgenic mouse models. TNF-mediated inflammatory arthritis was significantly attenuated in the absence of functional RANKL. Notably, TNF overexpression could not compensate for RANKL-mediated osteopetrosis, but promoted osteoclastogenesis between the pannus and bone interface, suggesting RANKL-independent mechanisms of osteoclastogenesis in inflamed joints. On the other hand, simultaneous overexpression of RANKL and TNF in double transgenic mice accelerated disease onset and led to severe arthritis characterized by significantly elevated clinical and histological scores as shown by aggressive pannus formation, extended bone resorption, and massive accumulation of inflammatory cells, mainly of myeloid origin. RANKL and TNF cooperated not only in local bone loss identified in the inflamed calcaneous bone, but also systemically in distal femurs as shown by microCT analysis. Proteomic analysis in inflamed ankles from double transgenic mice overexpressing human TNF and RANKL showed an abundance of proteins involved in osteoclastogenesis, pro-inflammatory processes, gene expression regulation, and cell proliferation, while proteins participating in basic metabolic processes were downregulated compared to TNF and RANKL single transgenic mice. Collectively, these results suggest that RANKL modulates modeled inflammatory arthritis not only as a mediator of osteoclastogenesis and bone resorption but also as a disease modifier affecting inflammation and immune activation.

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Heterogeneous nuclear ribonucleoprotein M promotes the progression of breast cancer by regulating the axin/β-catenin signaling pathway

Cited by 18 publications

References 29 publications

LDLRAD2 overexpression predicts poor prognosis and promotes metastasis by activating Wnt/β-catenin/EMT signaling cascade in gastric cancer

LDLRAD2 overexpression predicts poor prognosis and promotes metastasis by activating Wnt/β-catenin/EMT signaling cascade in gastric cancer

Chinese Herbal Formulas Miao-Yi-Ai-Tang Inhibits the Proliferation and Migration of Lung Cancer Cells through Targetingβ-Catenin/AXIN and Presents Synergistic Effect with Cisplatin Suppressing Lung Cancer

New Insights for RANKL as a Proinflammatory Modulator in Modeled Inflammatory Arthritis

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