Disturbing intracellular replication of Helicobacter Pylori by Sorafenib treatment in-vitro | ||||
| African Journal of Biological Sciences | ||||
| Articles in Press, Accepted Manuscript, Available Online from 27 December 2021 | ||||
| Document Type: Original Article | ||||
| DOI: 10.21608/ajbs.2021.107592.1026 | ||||
 View on SCiNiTO | ||||
| Authors | ||||
Tamer Roshdy  1; shimaa Ahmed Saleh2; Nasser Abbas3; Khalid Bassiouny3; Hany Khalil3
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| 1Department of Molecular Biology, Genetic Engineering and Biotechnology research institute, University of Sadat City, Egypt | ||||
| 2Molecular Biology, Genetic Engineering of Biotechnology Research Institute, University of Sadat City, Egypt | ||||
| 3Department of Molecular Biology, Genetic Engineering and Biotechnology Research Institute, University of Sadat City, Sadat City, Egypt | ||||
| Abstract | ||||
| Helicobacter pylori (H. pylori) is a Gram-negative, spiralling, microaerophilic bacteria that normally infect the stomach of humans . infection with H. pylori produces stomach inflammation which can develop to gastric ulcers of the stomach or the upper part of the small intestine. Several cellular signaling pathways such as mitogen activated protein kinases (MAPKs) and RNA activating factor 1 (RAF-1) signaling cascade may be involved in H. Pylori infection. MAPKs are a type of extracellular communication that consists of a chain of proteins that extends from cell receptors to nuclear DNA. MAPK signalling is usually triggered by cell receptors attaching to epidermal growth factors (EGF), also known as the growth factor pathway or extracellular signal-regulated kinase (ERK). By administering HeLa cells with Sorafenib (SOR), a systemic medication for malignant malignancies, we studied the possibility of inhibiting H. Pylori replication. In pre-treated and infected cells, the expression of RAF-1 and autophagy related 5 (Atg5) was monitored to see if targeting these factors can disrupt H. Pylori intracellular replication. Surprisingly, the relative expression of bacterial 16s ribosomal RNA in SOR-treated cells revealed a competitive suppression of bacterial replication (16srRNA). Furthermore, SOR therapy successfully controlled the expression of the Raf-1 and Atg5 genes without causing any toxicity. In addition, SOR therapy lowered the production of tumour necrosis factor (TNF-) in a dose and time-dependent manner. These data suggest that SOR can disrupt H. Pylori replication in HeLa cells by suppressing MAPK and autophagy signalling, with minimal TNF- generation from treated cells. | ||||
| Keywords | ||||
| Helicobacter pylori; Sorafenib; HeLa cell; MAPK signaling and autophagic process | ||||
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