Shiv K. Singh

ORCID: 0000-0002-5725-4058
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • Signaling Pathways in Disease
  • Pancreatic and Hepatic Oncology Research
  • Epigenetics and DNA Methylation
  • RNA modifications and cancer
  • Cancer Genomics and Diagnostics
  • Cancer Cells and Metastasis
  • Cancer-related gene regulation
  • Glioma Diagnosis and Treatment
  • Immune cells in cancer
  • Nuclear Receptors and Signaling
  • Renal and related cancers
  • Peptidase Inhibition and Analysis
  • MicroRNA in disease regulation
  • Aldose Reductase and Taurine
  • Macrophage Migration Inhibitory Factor
  • Phagocytosis and Immune Regulation
  • Cancer Immunotherapy and Biomarkers
  • Bone health and treatments
  • Molecular Biology Techniques and Applications
  • Bone Metabolism and Diseases
  • Neonatal Respiratory Health Research
  • Cancer-related Molecular Pathways
  • Cancer Mechanisms and Therapy
  • Cancer-related molecular mechanisms research
  • Cancer, Hypoxia, and Metabolism

Universitätsmedizin Göttingen
2014-2025

University of Göttingen
2016-2024

Nephrologisches Zentrum Goettingen
2021-2022

Philipps University of Marburg
2007-2020

Klinikum rechts der Isar
2014-2020

German Marine Research Consortium
2020

Technical University of Munich
2020

Target (Germany)
2020

St. Joseph's Hospital and Medical Center
2015-2019

Barrow Neurological Institute
2015-2019

Abstract Cancer-associated inflammation is a molecular key feature in pancreatic ductal adenocarcinoma. Oncogenic KRAS conjunction with persistent known to accelerate carcinogenesis, although the underlying mechanisms remain poorly understood. Here, we outline novel pathway whereby transcription factors NFATc1 and STAT3 cooperate epithelial cells promote KrasG12D-driven carcinogenesis. activation induced by itself accelerates inflammation-induced carcinogenesis KrasG12D mice, whereas genetic...

10.1158/2159-8290.cd-13-0593 article EN Cancer Discovery 2014-04-03

Objectives Non-alcoholic fatty liver disease (NAFLD) can persist in the stage of simple hepatic steatosis or progress to steatohepatitis (NASH) with an increased risk for cirrhosis and cancer. We examined mechanisms controlling progression severe NASH order develop future treatment strategies this disease. Design NFATc1 activation regulation was livers from patients NAFLD, cultured primary hepatocytes transgenic mice differential hepatocyte-specific expression transcription factor ( Alb-cre,...

10.1136/gutjnl-2021-325013 article EN cc-by-nc Gut 2022-04-01

One of the most deadly and aggressive cancers in world, pancreatic ductal adenocarcinoma (PDAC), typically manifests at an advanced stage. PDAC is becoming more common, by year 2030, it expected to overtake lung cancer as second greatest cause cancer-related death. The poor prognosis can be attributed a number factors, including difficulties early identification, probability curative radical resection, limited response chemotherapy radiotherapy, its immunotherapy resistance. Furthermore,...

10.3389/fimmu.2024.1323198 article EN cc-by Frontiers in Immunology 2024-02-07

Recent studies have thoroughly described genome-wide expression patterns defining molecular subtypes of pancreatic ductal adenocarcinoma (PDAC), with different prognostic and predictive implications. Although the reversible nature key regulatory transcription circuits two extreme PDAC subtype lineages "classical" "basal-like" suggests that states are not permanently encoded but underlie a certain degree plasticity, pharmacologically actionable drivers identity remain elusive. Here, we...

10.1158/0008-5472.can-20-0672 article EN Cancer Research 2020-09-09

In glioblastoma, invasion and proliferation are presumed to be mutually exclusive events; however, the molecular mechanisms that mediate this switch at cellular level remain elusive. Previously, we have shown phospho-OLIG2, a central-nervous-system-specific transcription factor, is essential for tumor growth proliferation. Here, show modulation of OLIG2 phosphorylation can trigger between invasion. Glioma cells with unphosphorylated OLIG2S10, S13, S14 highly migratory invasive, both in vitro...

10.1016/j.celrep.2016.06.045 article EN cc-by-nc-nd Cell Reports 2016-07-01

Missense p53 mutations (mutp53) occur in approx. 70% of pancreatic ductal adenocarcinomas (PDAC). Typically, mutp53 proteins are aberrantly stabilized by Hsp90/Hsp70/Hsp40 chaperone complexes. Notably, stabilization is a precondition for specific alleles to acquire powerful neomorphic oncogenic gain-of-functions (GOFs) that promote tumor progression solid cancers mainly increasing invasion and metastasis. In colorectal cancer (CRC), we recently established the common hotspot mutants...

10.3389/fonc.2021.642603 article EN cc-by Frontiers in Oncology 2021-06-11

We aimed to investigate the mechanistic, functional, and therapeutic role of glycogen synthase kinase 3β (GSK-3β) in regulation activation proinflammatory oncogenic transcription factor nuclear activated T cells (NFATc2) pancreatic cancer. IHC, qPCR, immunoblotting, immunofluorescence microscopy, proliferation assays were used analyze mouse human tissues cell lines. Protein-protein interactions promoter analyzed by coimmunoprecipitation, DNA pulldown, reporter, ChIP assays. Preclinical...

10.1158/1535-7163.mct-15-0309 article EN Molecular Cancer Therapeutics 2016-01-29

Background: The tumor microenvironment (TME) is composed of fibro-inflammatory cells and extracellular matrix (ECM) components. However, the exact contribution various TME compartments towards therapeutic response unknown. Here, we aim to dissect specific tumor-associated macrophages (TAMs) drug delivery in pancreatic ductal adenocarcinoma (PDAC). Methods: effect gemcitabine was assessed human murine macrophages, stellate (hPSCs), (L3.6pl, BxPC3 KPC) vitro. metabolism analyzed by liquid...

10.3390/cancers12071978 article EN Cancers 2020-07-20

The advent of high-throughput sequencing techniques has recently provided an astonishing insight into the composition and function human microbiome. Next-generation (NGS) become gold standard for advanced microbiome analysis; however, 3rd generation real-time sequencing, such as Oxford Nanopore Technologies (ONT), enables rapid from several kilobases to >2 Mb with high resolution. Despite wide availability enormous potential clinical translational applications, ONT is poorly standardized in...

10.1128/msystems.00750-21 article EN mSystems 2021-08-24

Human Surfactant Protein (SP-D) is a potent innate immune molecule, which emerging as key molecule in the recognition and clearance of altered non-self targets. Previous studies have shown that recombinant fragment human SP-D (rfhSP-D) induced apoptosis via p53 mediated pathway an eosinophilic leukemic cell line, AML14.3D10. Here, we report ability rfhSP-D to induce TNF-α/Fas-mediated regardless status pancreatic adenocarcinoma using Panc-1 (p53mt), MiaPaCa-2 Capan-2 (p53wt) lines. Treatment...

10.3389/fimmu.2018.01126 article EN cc-by Frontiers in Immunology 2018-06-04

Abstract Osteoprotegerin (OPG) is a decoy receptor for activator of NF‐κB ligand (RANKL) and TNF‐related apoptosis‐inducing (TRAIL). While RANKL essential osteoclastogenesis facilitates breast cancer migration into bone, TRAIL promotes apoptosis. We analyzed the expression OPG its modulation in estrogen receptor‐positive MCF‐7 cells receptor‐negative MDA‐MB‐231 cells. In both cells, mRNA levels protein secretion were dose‐ time‐dependently enhanced by interleukin (IL)‐1β suppressed...

10.1002/jcb.22232 article EN Journal of Cellular Biochemistry 2009-06-18

The aminobisphosphonate zoledronic acid has elicited significant attention due to its remarkable anti-tumoral activity, although detailed mechanism of action remains unclear. Here, we demonstrate the existence a nuclear GSK-3β-NFATc2 stabilization pathway that promotes breast and pancreatic cancer growth in vitro vivo serves as bona fide target acid. Specifically, serine/threonine kinase GSK-3β stabilizes NFATc2 through phosphorylation serine-rich SP2 domain, thus protecting transcription...

10.1074/jbc.m110.197533 article EN cc-by Journal of Biological Chemistry 2011-06-01

Pancreatic Ductal Adenocarcinoma (PDAC) represents a lethal malignancy with consistently poor outcome. Besides mutations in PDAC driver genes, the aggressive tumor biology of disease and its remarkable therapy resistance are predominantly installed by potentially reversible epigenetic dysregulation. However, regulators act context-dependent manner opposing implication on progression, thus critically determining therapeutic efficacy targeting. Herein, we aimed at exploring molecular...

10.3390/cancers14143451 article EN Cancers 2022-07-15
Coming Soon ...