The inhibition effect of natural food supplement active ingredients on TP63 carcinoma cell
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ORIGINAL PAPER
The inhibition effect of natural food supplement active ingredients on TP63 carcinoma cell Faik Gökalp1 Received: 20 October 2020 / Accepted: 14 November 2020 / Published online: 22 November 2020 © Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract In pancreatic cancer, the activities of inhibitory agents were investigated using docking, since the inhibition of TP63, which plays an important role in the spread of cancer with metastasis, in preventing the proliferation and proliferation of this type of cancer. It has been shown that the active ingredients in some plants used as traditional medicines have an inhibitory effect on this cancer type in preventing growth, reproduction and spread. These computational results guide experimental studies, preventing time and item loss; It is an important study in terms of choosing and using the right active substances. Keywords TP63 carcinoma cell · Docking · Thymol · Carvacrol · Tymoquinone Abbreviations DAS Diallyl sulfide DADS Diallyl disulfide DAS Diallyl sulfide DATS Diallyl trisulfide HNSCC Neck squamous cell carcinomas EMT Epithelial-mesenchymal transition LSCC Lung squamous cell carcinoma PC Pancreatic cancer TP63 Tumor protein p63 (also known simply as p63)
Introduction TP63 is a master regulator for essential role in epidermal differentiation [1]. It has also played an important role in connecting methylation genes and expression genes [2]. Tp63 is found to be highly expressed in metaplastic carcinomas of the breast with spindle cell or squamous differentiation [3]. It has frequently amplified or overexpressed in primary head and neck squamous cell carcinomas (HNSCC) [4]. Candidate genes close to these SNPs include MYC; TP63 (which encodes p63); prostate stem.
* Faik Gökalp [email protected] 1
Cell [5]. P63 proteins have an important function in the stratification of the squamous epithelium and differentiation of mature keratinocytes; the stability of this protein is regulated mainly by ubiquitin-dependent proteasomal degradation. Apart from some protein kinases, other protein types are also involved in the regulation of p63 protein stability, and these regulators respond to various extracellular signals, causing changes in p63 protein levels to affect many different biological processes. [6]. Clinical results in (Lung squamous cell carcinoma) LSCC patients through regulation of tumor protein p63 (TP63) ubiquitination can provide a key to the development of sensitive medicine for TP63 [7]. TP53/TP63/TP73 family had a similar DNA-binding domain that acts as a tumor s uppressor5 [8]. TP63 is required to maintain stem cell pluripotency and suppresses the metastatic potential of cancer cells through multiple mechanism [9]. Pancreatic cancer (PC) remains the leading cause of cancer-related death worldwide. PC metastasis is the result of a complex series of events involving epithelial-mesenchymal transition (EMT) that increases tumor cell invasiveness. The compound called MiR-301a functions as an oncogene in mul
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