CARMA3 regulates the invasion, migration, and apoptosis of non-small cell lung cancer cells by activating NF-кB and suppressing the P38 MAPK signaling pathway

Xia, Zhixiu; Li, Z.X.; Zhang, M.; Sun, Liqing; Zhang, Q.F.; Qiu, Xueshan

doi:10.1016/j.yexmp.2015.10.004

Cited by 22 publications

(15 citation statements)

References 35 publications

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“…A number of studies have shown that MAPKs (jNK1/2, ERK1/2, and p38) are involved in the growth, migration, and alterations in MMPs activity (24,25) in various cancers including lung, prostate, colorectal and ovarian cancer (26)(27)(28)(29)(30). Furthermore, the ERK signaling pathway in addition to the p38 signaling pathway may regulate numerous factors that are associated with cancer progression and poor prognosis in NSCLC (31)(32)(33).…”

Section: Discussionmentioning

confidence: 99%

Fibroblast growth factor 18 promotes proliferation and migration of H460 cells via the ERK and p38 signaling pathways

et al. 2016

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Abstract.Recently, fibroblast growth factor 18 (FGF18) expression was reported to be upregulated in colon cancer and ovarian cancer, and increased expression of FGF18 mRNA and protein is associated with tumor progression and poor overall survival in patients; however, its role in lung cancer remains to be explored. In the present study, the effect and underlying molecular mechanisms of FGF18 on H460 cells were investigated. Cell proliferation and cell cycle alterations were detected using a 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide assay and flow cytometry. A wound healing assay was conducted to detect cell migration. Reverse transcription-quantitative polymerase chain reaction and western blotting were performed to measure extracellular signal-regulated kinase (ERK), p38 and matrix metalloproteinase 26 (MMP26) expression. Knockdown of FGF18 using short interfering RNA (siRNA-FGF18) suppressed H460 cell proliferation, inhibited cell migration via the downregulation of MMP26 levels, with siRNA-FGF18 additionally inhibiting the ERK and p38 signaling pathway. The present study indicates that FGF18 serves an essential role in the growth and migration of non-small cell lung cancer (NSCLC) cells by regulating the ERK, p38 signaling pathways and MMP26 protein levels, suggesting that FGF18 may be a potential molecular drug target for the treatment NSCLC.

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Section: Discussionmentioning

confidence: 99%

Fibroblast growth factor 18 promotes proliferation and migration of H460 cells via the ERK and p38 signaling pathways

et al. 2016

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“…CARD11 (CARMA1), expressed in lymphoid cells, is activated upon B-and T-cell receptor engagement, and gain-of-function (GoF) mutations in the genes encoding CARD11, Bcl10, and Malt1 have been associated with a number of lymphoid malignancies (Gaide, et al, 2002;Juilland and Thome, 2016;Pomerantz et al, 2002;Wang et al, 2002). Similarly, CARD10 (CARMA3), expressed in epithelial tissue and activated by G protein-coupled receptor stimulation, has been linked to the progression of various carcinomas (Du et al, 2014;Pan et al, 2016;Xia et al, 2016;Xie et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

CARD14 Gain-of-Function Mutation Alone Is Sufficient to Drive IL-23/IL-17–Mediated Psoriasiform Skin Inflammation In Vivo

Mellett

Meier

Mohanan

et al. 2018

Journal of Investigative Dermatology

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Rare autosomal dominant mutations in the gene encoding the keratinocyte signaling molecule CARD14, have been associated with an increased susceptibility to psoriasis, but the physiological impact of CARD14 gain-of-function mutations remains to be fully determined in vivo. Here, we report that heterozygous mice harboring a CARD14 gain-of-function mutation (Card14ΔE138) spontaneously develop a chronic psoriatic phenotype with characteristic scaling skin lesions, epidermal thickening, keratinocyte hyperproliferation, hyperkeratosis, and immune cell infiltration. Affected skin of these mice is characterized by elevated expression of anti-microbial peptides, chemokines, and cytokines (including T helper type 17 cell-signature cytokines) and an immune infiltrate rich in neutrophils, myeloid cells, and T cells, reminiscent of human psoriatic skin. Disease pathogenesis was driven by the IL-23/IL-17 axis, and neutralization of IL-23p19, the key cytokine in maintaining T helper type 17 cell polarization, significantly reduced skin lesions and the expression of antimicrobial peptides and proinflammatory cytokines. Therefore, hyperactivation of CARD14 alone is sufficient to orchestrate the complex immunopathogenesis that drives T helper type 17-mediated psoriasis skin disease in vivo.

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“…In addition, the RNA sequencing data revealed a gene involved in nitrogen metabolism, CPS1, as a potential downstream gene regulated by CARD10. Additionally, the RNA sequencing data revealed several other genes that have been reported to be regulated by the NF‐κB pathway, such as IL6, MAPK1, SSAT, HK2 and GLUT1 . Thus, we hypothesized that CPS1 may also be regulated via the NF‐κB pathway.…”

Section: Discussionmentioning

confidence: 92%

“…Additionally, the RNA sequencing data revealed several other genes that have been reported to be regulated by the NF-κB pathway, such as IL6, MAPK1, SSAT, HK2 and GLUT1. [24][25][26][27][28] Thus, we hypothesized that CPS1 may also be regulated via the NF-κB pathway.…”

Section: Discussionmentioning

confidence: 99%

Caspase recruitment domain family member 10 regulates carbamoyl phosphate synthase 1 and promotes cancer growth in bladder cancer cells

Liu

Zhang

et al. 2019

J Cellular Molecular Medi

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Bladder cancer, which can be divided into non‐muscle‐invasive and muscle‐invasive bladder cancer, is the most common urinary cancer in the United States. Caspase recruitment domain family member 10 (CARD10), also named CARD‐containing MAGUK protein 3 (CARMA3), is a member of the CARMA family and may activate the nuclear factor kappa B (NF‐κB) pathway. We utilized RNA sequencing and metabolic mass spectrometry to identify the molecular and metabolic feature of CARD10. The signalling pathway of CARD10 was verified by Western blotting analysis and functional assays. RNA sequencing and metabolic mass spectrometry of CARD10 knockdown identified the metabolic enzyme carbamoyl phosphate synthase 1 (CPS1) in the urea cycle as the downstream gene regulated by CARD10. We confirmed that CARD10 affected cell proliferation and nucleotide metabolism through regulating CPS1. We indicated that CARD10 promote bladder cancer growth via CPS1 and maybe a potential therapeutic target in bladder cancer.

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CARMA3 regulates the invasion, migration, and apoptosis of non-small cell lung cancer cells by activating NF-кB and suppressing the P38 MAPK signaling pathway

Cited by 22 publications

References 35 publications

Fibroblast growth factor 18 promotes proliferation and migration of H460 cells via the ERK and p38 signaling pathways

Fibroblast growth factor 18 promotes proliferation and migration of H460 cells via the ERK and p38 signaling pathways

CARD14 Gain-of-Function Mutation Alone Is Sufficient to Drive IL-23/IL-17–Mediated Psoriasiform Skin Inflammation In Vivo

Caspase recruitment domain family member 10 regulates carbamoyl phosphate synthase 1 and promotes cancer growth in bladder cancer cells

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