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Pancreatic cancer cells treated with anlotinib

ABSTRACT: Aberrant regulation of angiogenesis involves in the growth and metastasis of tumors, but angiogenesis inhibitors fail to improve overall survival of pancreatic cancer patients in previous phase III clinical trials. A comprehensive knowledge of the mechanism of angiogenesis inhibitors against pancreatic cancer is helpful for clinical purpose and for the selection of patients who might benefit from the inhibitors. In this work, multi-omics analyses (transcriptomics, proteomics and phosphoproteomics profiling) were carried to delineate the mechanism of anlotinib, a novel angiogenesis inhibitor, against pancreatic cancer cells.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture

SUBMITTER: Zewen Song

LAB HEAD: Zewen Song

PROVIDER: PXD023344 | Pride | 2021-09-09

REPOSITORIES: Pride

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Publications

Multi-Omics Analysis of Anlotinib in Pancreatic Cancer and Development of an Anlotinib-Related Prognostic Signature.

Zhang Xi X Liu Yang Y Zhang Zhen Z Tan Juan J Zhang Junjun J Ou Hao H Li Jie J Song Zewen Z

Frontiers in cell and developmental biology 20210304

Aberrant regulation of angiogenesis involves in the growth and metastasis of tumors, but angiogenesis inhibitors fail to improve overall survival of pancreatic cancer patients in previous phase III clinical trials. A comprehensive knowledge of the mechanism of angiogenesis inhibitors against pancreatic cancer is helpful for clinical purpose and for the selection of patients who might benefit from the inhibitors. In this work, multi-omics analyses (transcriptomics, proteomics, and phosphoproteomi ...[more]

PMID: 33748143

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Phosphoproteomics Data of pancreatic cancers cells treated with anlotinib

Project description:Aberrant regulation of angiogenesis involves in the growth and metastasis of tumors, but angiogenesis inhibitors fail to improve overall survival of pancreatic cancer patients in previous phase III clinical trials. A comprehensive knowledge of the mechanism of angiogenesis inhibitors against pancreatic cancer is helpful for clinical purpose and for the selection of patients who might benefit from the inhibitors. In this work, multi-omics analyses (transcriptomics, proteomics and phosphoproteomics profiling) were carried to delineate the mechanism of anlotinib, a novel angiogenesis inhibitor, against pancreatic cancer cells.

2021-09-09 | PXD023345 | Pride

Comparative analysis of serum proteins between hepatitis B virus genotype B and C infection DIA-based quantitative proteomics

Project description:Hepatitis B virus (HBV) is an enveloped, coated, non-cytopathic and hepatotropic partially double-stranded DNA virus in the family Hepadnaviridae genus Orthohepadnavirus. Despite significant progress in the availability of safe vaccines and antiviral therapies against HBV, it still affects approximately 257 million people worldwide and is responsible for about 887,000 deaths per year around the world [4]. HBV infection, which are associated with acute and chronic liver failure responses to viruses attacked the liver, can result in inactive carrier state, chronic hepatitis, or fulminant hepatitis and put them at high risk to develop advanced liver fibrosis and cirrhosis, and even hepatocellular cancer. Many viral factors, which could affect the disparity of clinical outcomes or disease prognosis during chronic HBV infection, have been reported in previous studies; among them, the viral genotype, as well as HBV mutations ascribing the virus to a certain phenotype, was reported to be the most important factor influencing viral pathogenesis, including the change of host immune recognition, the enhanced virulence with increased HBV replication and the facilitation of cell attachment or penetration.

2022-02-17 | PXD025968 | Pride

Serum proteomic profiling in patients with advanced Schistosoma japonicum-induced hepatic fibrosis

Project description:Background: Schistosoma japonicum (S. japonicum) is a parasitic flatworm that is the aetiological agent of human schistosomiasis, an important cause of hepatic fibrosis. Schistosomiasis-induced hepatic fibrosis is a consequence of the highly fibrogenic nature of egg-induced granulomatuous lesions, the main pathogenic factor of schistosomiasis. Although global awareness of the association between schistosomiasis-indued hepatic fibrosis and s. japonicum infection is increasing, little is known about the molecular differences associated with rapid progression to schistosomiasis in cirrhotic patients. Methods: We systematically used data-independent acquisition (DIA)-based liquid chromatography-mass spectrometry to identify differentially expressed proteins in serum samples from patients with advanced S. japonicum-induced hepatic fibrosis. Results: On the basis of our analysis, we identified 1,144 proteins, among which 66 were differentially expressed between the healthy control and SHF-F2 groups and 214 were differentially expressed between the SHF-F2 and SHF-F4 groups (up- or downregulation of at least 1.5-fold in serum samples). Furthermore, our results indicated that two selected proteins (C1QA and CFD) are potential biomarkers for distinguishing patients with SHF-F2 and SHF-F4 resulting from S. japonicum infection. Conclusions: This report is the first to provide a global proteomic profile of serum samples from patients with advanced S. japonicum-induced hepatic fibrosis. C1QA and CFD are potentially diagnostic markers for patients with SHF-F2 and SHF-F4 resulting from S. japonicum infection, although further large-scale studies are needed. Our DIA-based quantitative proteomic analysis revealed molecular differences among individuals with different stages of advanced S. japonicum-induced hepatic fibrosis and might provide fundamental information for further detailed investigations.

2022-09-06 | PXD025224 | Pride

Pathogenic Bacteria Exploit Transferrin Receptor Transcytosis to Penetrate the Blood‒Brain Barrier

Project description:In this study, we present evidence showing that the infection with the major meningitis-causing bacteria, NMEC, GBS and SPN, activates the same fusion process of bacteria-containing vesicles (BCVs) with TfR vesicles, which enables those bacteria to exploit TfR transcytosis to penetrate the BBB, and illustrate the details of this process in HBMECs and mouse models.

2023-10-24 | PXD039060 | Pride

Pharmacological Targeting of Casein Kinase 1δ Suppresses Oncogenic NRAS-Driven Melanoma

Project description:Activating mutations in NRAS account for 15-20% of melanoma, yet effective anti-NRAS therapies are still lacking. In this study, we unveil the casein kinase 1δ (CK1δ) as an uncharacterized regulator of oncogenic NRAS mutations, specifically Q61R and Q61K, which are the most prevalent NRAS mutations in melanoma. The genetic ablation or pharmacological inhibition of CK1δ markedly destabilizes NRAS mutants and suppresses their oncogenic functions. Moreover, we identify USP46 as a bona fide deubiquitinase of NRAS mutants. Mechanistically, CK1δ directly phosphorylates USP46 and activates its deubiquitinase activity towards NRAS mutants, thus promoting oncogenic NRAS-driven melanocyte malignant transformation and melanoma progression in vitro and in vivo. Our findings underscore the significance of the CK1δ-USP46 axis in stabilizing oncogenic NRAS mutants and provide preclinical evidence that targeting this axis holds promise as a therapeutic strategy for human melanoma harboring NRAS mutations.

2024-09-19 | PXD051431 | Pride

Two novel zinc and cobalt-responsive proteins in marine eukaryotic phytoplankton and implications for Zn scarcity in the surface oceans

Project description:Observations of scarce surface ocean concentrations of dissolved zinc (Zn) have raised the possibility that Zn may co-limit the growth of oceanic phytoplankton, yet testing this hypothesis has been difficult because Zn is highly prone to contamination. Biomarkers of micro-nutrient stress can serve as an alternate means to assay, though biomarker proteins for Zn stress in marine algae are currently uncharacterized. In this study we identified two Zn-responsive proteins in four marine diatom species that became abundant under Zn and Co limitation, but were scarce or undetectable in replete conditions. We refer to these proteins as ZCRP-A and ZCRP-B (Zn/Co Responsive Protein A and B). Sequence similarity of ZCRP-A to the Escherichia coli model COG0523 protein YjiA suggests a Zn2+ binding capability using conserved metal binding sites. Cellular localization by fluorescent tagging and overexpression of these proteins showed that ZCRP-B is part of a membrane-bound transport complex and that ZCRP-A serves as a Zn/Co chaperone with a chloroplastic target. These results imply that ZCRP-A and ZCRP-B are important in intracellular Zn trafficking and high-affinity transport, respectively. Metaproteomic detection of ZCRP-A and ZCRP-B homologs in a variety of eukaryotic protists along a South Pacific Ocean transect demonstrated that both proteins were more abundant in the euphotic zone (0-200m) where dZn and dCo were scarce. These findings describe widely distributed marine algal proteins linked to Zn and Co metabolism that together contribute to our understanding of Zn homeostasis in important marine phytoplankton.

2022-03-02 | PXD026953 | Pride

Mechanism of chaperone coordination during cotranslational protein folding in bacteria

Project description:Protein folding is assisted by molecular chaperones that bind nascent polypeptides during mRNA translation. Several structurally-distinct classes of chaperones promote de novo folding, suggesting that their activity is coordinated at the ribosome. Here we use biochemical reconstitution and structural proteomics to explore the molecular basis for cotranslational chaperone action in bacteria. We find that chaperone binding is disfavoured close to the ribosome, allowing folding to precede chaperone recruitment. Trigger factor subsequently recognises compact folding intermediates exposing extensive non-native surface and dictates DnaJ access to nascent chains. DnaJ uses a large surface to bind structurally diverse intermediates, and recruits DnaK to solvent-accessible sites in a sequence non-specific manner. Neither Trigger factor, DnaJ nor DnaK destabilize cotranslational folding intermediates. Instead, the chaperones collaborate to create a protected space for protein maturation that extends well beyond the ribosome exit tunnel. Our findings show how the chaperone network selects and modulates cotranslational folding intermediates.

2024-07-03 | PXD048638 | Pride

Comparative TMT-based quantitative proteomic analysis of the Tachaea chinensis isopod during parasitism

Project description:Parasitic isopods perforate and attach to the host integument via the mandibles, then feed on hemolymph and exudate from the wounds. Such isopods attack a variety of commercially important fish and crustacean hosts. Like other hematophagous parasites, isopods employ biomolecules that inhibit host blood conglutination and defense. In the present study, a tandem mass tag-based quantitative proteomic approach was used to identify differentially expressed proteins in Tachaea chinensis parasites of shrimp, by comparing parasitic (fed) and pre-parasitic (unfed) individuals. We identified 888 proteins from 1510 total peptides, with a significant difference in 129 between the fed and unfed groups. Among these, 37 were upregulated and 92 were downregulated in unfed T. chinensis. This indicates that T. chinensis may require more energy before parasitism during its search for a host. In addition, as is the case for other blood-sucking parasites, it might secrete antihemostatic, anti-inflammatory and immunomodulatory molecules to facilitate blood meal acquisition. Our study is the first to use a TMT-based proteomic approach to analyze the proteome of isopod parasites, and our results will facilitate our understanding of the molecular mechanisms of isopod parasitism on crustaceans.

2020-05-26 | PXD015247 | Pride

Nitric Oxide Enhances Resistance to PEG-induced Water Deficiency is Associated with the Primary Photosynthesis Reaction in Triticum aestivum L.

Project description:Photosynthesis is affected by water deficiency (WD) stress, and nitric oxide (NO) is a free radical that participates in the photosynthesis process. Previous studies have suggested that NO regulates the excitation energy distribution of photosynthesis under WD stress. Here, quantitative phosphoproteomic profiling was conducted using isobaric tags for relative and absolute quantitation. Differentially phosphorylated protein species (DEPs) were identified in leaves of NO or polyethylene glycol (PEG)-treated wheat seedlings (D) and in control seedlings, 2,257 unique phosphorylated peptides and 2,416 phosphorylation sites were identified from 1,396 unique phosphoproteins. Of these, 96 DEPs displayed significant changes (≥ 1.50-fold, p < 0.01). These DEPs are involved in photosynthesis and signal transduction, etc. Furthermore, phosphorylation of several DEPs were up-regulated by both D and NO treatments, but down-regulated only in NO treatment. These differences affected the chlorophyll A-B binding protein, chloroplast post-illumination chlorophyll fluorescence increase protein, and SNT7, implying that NO indirectly regulated the absorption and transport of light energy in photosynthesis in response to WD stress. The significant difference of chlorophyll (Chl) content, Chl a fluorescence transient, photosynthesis index, and trapping and transport of light energy further indicated that exogenous NO under D stress enhanced the primary reaction of photosynthesis compared to D treatment. A putative pathway is proposed to elucidate NO regulation of the primary reaction of photosynthesis under WD.

2019-11-14 | PXD010724 | Pride

Species-specific metabolic reprogramming in human and mouse microglia during inflammatory pathway induction

Project description:Metabolic reprogramming is a hallmark of the immune cells in response to inflammatory stimuli. This metabolic process involves a switch from oxidative phosphorylation (OXPHOS)to glycolysis, or alterations in other metabolic pathways. However, most of the experimental findings have been acquired in murine immune cells and little is known about the metabolic reprogramming of human microglia. In this study, we investigated the transcriptomic and metabolic profiles of mouse and iPSC-derived human microglia challenged with the TLR4 agonist LPS. We found that both species displayed a metabolic shift and an overall increased glycolytic gene signature in response to LPS treatment. The metabolic reprogramming was characterized by the upregulation of hexokinases in mouse microglia and phosphofructokinases in human microglia. This study provides the first direct comparison of energy metabolism between mouse and human microglia, highlighting the species-specific pathways involved in immunometabolism and the importance of considering these differences in translational research.

2023-09-02 | PXD043836 | Pride