The role of adrenomedullin in the pathogenesis of gastric cancer

Qiao, Fuhao; Fang, Jian; Xu, Jinfeng; Zhao, Wenqiu; Ni, Ying; Akuo, Bufugdi Andreas; Zhang, Wei; Liu, Yun; Ding, Fangfang; Li, Guanlin; Liu, Baoguo; Wang, Hua; Shao, Shihe

doi:10.18632/oncotarget.18881

Cited by 12 publications

(12 citation statements)

References 37 publications

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“…Furthermore, the expression levels of AM and its receptors are inordinately elevated in gastric cancer as compared to the adjacent non-tumor gastric tissues [ 128 ], and increased AM expression results in the proliferation of tumor cells, tumor invasion, and metastasis.…”

Section: Pathophysiological Involvement Of Adrenomedullin/pamp In The...mentioning

confidence: 99%

Adrenomedullin: Not Just Another Gastrointestinal Peptide

Martínez-Herrero

Martı́nez

2022

Biomolecules

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Adrenomedullin (AM) and proadrenomedullin N-terminal 20 peptide (PAMP) are two bioactive peptides derived from the same precursor with several biological functions including vasodilation, angiogenesis, or anti-inflammation, among others. AM and PAMP are widely expressed throughout the gastrointestinal (GI) tract where they behave as GI hormones, regulating numerous physiological processes such as gastric emptying, gastric acid release, insulin secretion, bowel movements, or intestinal barrier function. Furthermore, it has been recently demonstrated that AM/PAMP have an impact on gut microbiome composition, inhibiting the growth of bacteria related with disease and increasing the number of beneficial bacteria such as Lactobacillus or Bifidobacterium. Due to their wide functions in the GI tract, AM and PAMP are involved in several digestive pathologies such as peptic ulcer, diabetes, colon cancer, or inflammatory bowel disease (IBD). AM is a key protective factor in IBD onset and development, as it regulates cytokine production in the intestinal mucosa, improves vascular and lymphatic regeneration and function and mucosal epithelial repair, and promotes a beneficial gut microbiome composition. AM and PAMP are relevant GI hormones that can be targeted to develop novel therapeutic agents for IBD, other GI disorders, or microbiome-related pathologies.

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Section: Pathophysiological Involvement Of Adrenomedullin/pamp In The...mentioning

confidence: 99%

Adrenomedullin: Not Just Another Gastrointestinal Peptide

Martínez-Herrero

Martı́nez

2022

Biomolecules

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“…Furthermore, the observed ADM upregulation is intriguing and has a potentially important translational consequence. In addition to ADM activation upon hypoxia [ 45 – 51 ], ADM was also shown to act as growth factor, prevent apoptosis-mediated cell death, increase tumour cell motility and metastasis and induce angiogenesis in various cancer types [ 47 – 49 , 51 , 53 – 59 ]. Of further importance, it has been reported that hypoxia, which can activate ADM [ 45 – 51 ], induces resistance to ALK inhibitors in non-small cell lung cancer [ 60 ] and that ADM expression levels are increased in tyrosine kinase inhibitor sunitinib resistant renal cell carcinoma [ 61 ].…”

Section: Resultsmentioning

confidence: 99%

Early and late effects of pharmacological ALK inhibition on the neuroblastoma transcriptome

et al. 2017

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BackgroundNeuroblastoma is an aggressive childhood malignancy of the sympathetic nervous system. Despite multi-modal therapy, survival of high-risk patients remains disappointingly low, underscoring the need for novel treatment strategies. The discovery of ALK activating mutations opened the way to precision treatment in a subset of these patients. Previously, we investigated the transcriptional effects of pharmacological ALK inhibition on neuroblastoma cell lines, six hours after TAE684 administration, resulting in the 77-gene ALK signature, which was shown to gradually decrease from 120 minutes after TAE684 treatment, to gain deeper insight into the molecular effects of oncogenic ALK signaling.AimHere, we further dissected the transcriptional dynamic profiles of neuroblastoma cells upon TAE684 treatment in a detailed timeframe of ten minutes up to six hours after inhibition, in order to identify additional early targets for combination treatment.ResultsWe observed an unexpected initial upregulation of positively regulated MYCN target genes following subsequent downregulation of overall MYCN activity. In addition, we identified adrenomedullin (ADM), previously shown to be implicated in sunitinib resistance, as the earliest response gene upon ALK inhibition.ConclusionsWe describe the early and late effects of ALK inhibitor TAE684 treatment on the neuroblastoma transcriptome. The observed unexpected upregulation of ADM warrants further investigation in relation to putative ALK resistance in neuroblastoma patients currently undergoing ALK inhibitor treatment.

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“…ADM has been reported to be ubiquitously expressed and participate in multiple pathophysiological processes, including renal failure, hypertension, septic shock, and tumorigenesis (Figueira & Israel, ; Hirose et al, ; MV et al, ; Ochoa‐Callejero et al, ; Qiao et al, ). Notably, ADM can be regarded as a target for the treatment of central nervous system (CNS) diseases, as its roles in alleviating neuronal damages have been demonstrated in several animal experiments (Chaung et al, ; S. M. Wang & Yang, ; Xia, Yin, Borlongan, Chao, & Chao, ).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐26b inhibits oligodendrocyte precursor cell differentiation by targeting adrenomedullin in spinal cord injury

Cheng

Wang

Yao

et al. 2019

Journal Cellular Physiology

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Oligodendrocyte precursor cells (OPCs) serve as a reservoir of newborn oligodendrocytes (OLs) in pathological and homeostatic conditions. After spinal cord injury (SCI), OPCs are activated to generate myelinating OLs, contributing to remyelination and functional recovery; however, the underlying molecular mechanisms remain unclear. Here, microRNA-26b (miR-26b) expression in the spinal cord tissues of SCI rats was examined by real-time polymerase chain reaction analysis. The influences of miR-26b on locomotor recovery following SCI were assessed utilizing Basso, Beattie, and Bresnahan (BBB) scores. The effects of miR-26b on OPC differentiation were explored using immunofluorescence and western blot analyses in vitro and in vivo.The potential targets that are modulated by miR-26b were identified by bioinformatics, luciferase reporter assays, and western blot analyses. The effects of adrenomedullin (ADM) on OPC differentiation were explored in vitro using immunofluorescence and western blot analyses. We demonstrated that miR-26b was significantly downregulated after SCI. BBB scores showed that miR-26b exacerbated the locomotor function deficits induced by SCI. In vitro, miR-26b inhibited the differentiation of primary rat OPCs. In vivo, miR-26b suppressed OPC differentiation in SCI rats. Bioinformatics analyses and experimental detection revealed that miR-26b directly targeted ADM in OPCs. In addition, knockdown of ADM suppressed the differentiation of primary rat OPCs. Our study provides evidence that ADM may mediate miR-26b-inhibited OPC differentiation in SCI. K E Y W O R D S adrenomedullin, differentiation, microRNA-26b, oligodendrocyte precursor cells, spinal cord injury

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The role of adrenomedullin in the pathogenesis of gastric cancer

Cited by 12 publications

References 37 publications

Adrenomedullin: Not Just Another Gastrointestinal Peptide

Adrenomedullin: Not Just Another Gastrointestinal Peptide

Early and late effects of pharmacological ALK inhibition on the neuroblastoma transcriptome

MicroRNA‐26b inhibits oligodendrocyte precursor cell differentiation by targeting adrenomedullin in spinal cord injury

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