Data on differential pathogenic ability of Helicobacter pylori isolated from distinct gastric niches

Baral, Budhadev; Kashyap, Dharmendra; Varshney, Nidhi; Verma, Tarun; Jain, Ajay; Chatterji, Debi; Kumar, Vijay; Mishra, Amit Kumar; Kumar, Arvind; Jha, Hem Chandra

doi:10.1016/j.dib.2023.108981

Cited by 4 publications

(2 citation statements)

References 5 publications

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“…Genomic instability was examined in pEGFP-c1 and AURKA-wt exposed cells followed by treatment with kinase inhibitors. Brie y, cells were seeded in a 12-well plate and after reaching the desired con uency, cells were exposed with pEGFP-c1 and AURKA-wt followed by treatment with kinase inhibitors and further protocol according to previous literature [47]. The percentage of multinuclei and micronuclei was quanti ed by counting ~ 200 cells in 10 different elds.…”

Section: Genomic Instability Assaymentioning

confidence: 99%

Unveiling the therapeutic potential of Ponatinib and Imatinib against Aurora Kinase A in gastric cancer cells

Varshney

Kashyap

Saini

et al. 2023

Preprint

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Aurora kinase A (AURKA) is considered a promising therapeutic target because of its abnormal expression pattern in multiple cancers. Since AURKA possesses a high similarity in active binding site with other kinases, we attempted to investigate and rationalize several kinase inhibitors that are currently under preclinical and clinical settings. All such inhibitors were selected based on sequence and structural similarity of AURKA with other kinases. Molecular docking revealed that Ponatinib, Imatinib, GSK-2334470, CFI-400945, MK2 inhibitor 3, and Vemurafenib bound to AURKA with high affinity. Molecular Dynamic (MD) simulations were carried out to assess pocket druggability, and stability of the potential inhibitors with respect to binding free-energy calculations. The findings suggested stable binding, particularly, for Ponatinib and Imatinib with AURKA via Van der Waals interactions. We identified Leu139, Val147, Lys162, Tyr212, Gly216, Leu263, and Asp274 as hotspot residues for binding of the inhibitors. Further, in vitro analyses of Ponatinib and Imatinib along with positive control MLN8237 realized decrease in AURKA expression at genomic as well as protein level studies even after ectopic transfection of AURKA. Notably, these compounds also reduced the expression of related signaling molecules β-catenin, STAT3 and its phosphorylation and NF-𝜿B and its phosphorylation. Beside the negative influence exercised by inhibitors on the oncogenic effect such as cell proliferation and genomic instability, Ponatinib and Imatinib also induced apoptosis rescue by AURKA and enhanced the protein expression of apoptotic markers like Caspase 9, 8, 3 and PARP1. Our results suggest these compounds as promising molecules to be used against AURKA.

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Section: Genomic Instability Assaymentioning

confidence: 99%

Unveiling the therapeutic potential of Ponatinib and Imatinib against Aurora Kinase A in gastric cancer cells

Varshney

Kashyap

Saini

et al. 2023

Preprint

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“…8,9 Therefore, the coexistence of H. pylori and EBV enhanced the aggressiveness of GC by modulating the various signaling genes' transcripts and proteins such as protein p53 (p53), protein retinoblastoma (pRB), matrix metalloproteinases (MMPs), and cell-cycle regulators cyclin D1 (CCND1), Ak strain transforming (Akt), nuclear factor kappa B (NFkB), light chain 3B (LC3B), autophagy-related transcription factor 7 (ATG7), and so forth. [8][9][10] Systemic chemotherapy, radiotherapy, surgery, immunotherapy, and targeted therapy have proven efficacy in gastric adenocarcinoma; therefore, multidisciplinary treatment is paramount to treatment selection. 11 Several cytotoxic agents are active in advanced GC, including fluoropyrimidines, platinum, taxanes, and irinotecan.…”

Section: Introductionmentioning

confidence: 99%

Spectroscopic assessment of biomolecular changes in Helicobacter pylori and Epstein–Barr virus co‐infected gastric epithelial cells

Kashyap,

Tanwar,

Rani

et al. 2024

J Raman Spectroscopy

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Helicobacter pylori and Epstein–Barr Virus (EBV) are Group 1 carcinogens that can enhance gastric cancer progression. Bioactive substances extracted from plants can be effective therapeutic agents in cancer treatment. For example, Withania somnifera extract‐WSE reduces the Gankyrin oncoprotein, which is upregulated in the presence of H. pylori and EBV. The various biochemical and metabolic changes upon 24 hrs post‐infection followed by W. somnifera extract (WSE) treatment on gastric epithelial cells (AGS) can be studied using spectroscopic techniques. In the biomedical sciences, Raman and NMR spectroscopy have been extensively employed to interpret cellular alterations contributing to the onset of infection and the severity of gastric cancer. More specifically, alterations in cellular biochemical homeostasis are linked to the moieties of cholesterol, collagen, choline, carbohydrate, lipids, tyrosine, and phenylalanine. Further, we have found significantly elevated FWHM for carbohydrates, tumor associated protein, collagen, cholesterol, and cholesterol ester in the co‐infection model. We also looked into the potential correlation between these molecules using molecular network analysis and found several related factors that can be modulated through biomolecular levels. These molecules are crucial in several physiological functions, including cell division, cell proliferation, apoptosis, necrosis, cell migration, and lipid transport. Our study paves the pathway to study H. pylori and EBV co‐infection in human gastric epithelial cells and the therapeutic interventions of WSE in this scenario and highlights specific biomolecular alterations, which can be focused for further mechanistic investigations.

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Computational insights into VacA toxin inhibition: harnessing FDA-approved antibiotics against Helicobacter pylori

Kashyap,

Koirala,

Roy

et al. 2023

Journal of Biomolecular Structure and Dynamics

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Data on differential pathogenic ability of Helicobacter pylori isolated from distinct gastric niches

Cited by 4 publications

References 5 publications

Unveiling the therapeutic potential of Ponatinib and Imatinib against Aurora Kinase A in gastric cancer cells

Unveiling the therapeutic potential of Ponatinib and Imatinib against Aurora Kinase A in gastric cancer cells

Spectroscopic assessment of biomolecular changes in Helicobacter pylori and Epstein–Barr virus co‐infected gastric epithelial cells

Computational insights into VacA toxin inhibition: harnessing FDA-approved antibiotics against Helicobacter pylori

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