Abstract
The equine sarcoid is one of the most common neoplasias in the Equidae family. Despite the association of this tumor with the presence of bovine papillomavirus (BPV), the molecular mechanism of this lesion has not been fully understood. The transgenization of equine adult cutaneous fibroblast cells (ACFCs) was accomplished by nucleofection, followed by detection of molecular modifications using high-throughput NGS transcriptome sequencing. The results of the present study confirm that BPV-E4- and BPV-E1^E4-mediated nucleofection strategy significantly affected the transcriptomic alterations, leading to sarcoid-like neoplastic transformation of equine ACFCs. Furthermore, the results of the current investigation might contribute to the creation of in vitro biomedical models suitable for estimating the fates of molecular dedifferentiability and the epigenomic reprogrammability of BPV-E4 and BPV-E4^E1 transgenic equine ACFC-derived sarcoid-like cell nuclei in equine somatic cell-cloned embryos. Additionally, these in vitro models seem to be reliable for thoroughly recognizing molecular mechanisms that underlie not only oncogenic alterations in transcriptomic signatures, but also the etiopathogenesis of epidermal and dermal sarcoid-dependent neoplastic transformations in horses and other equids. For those reasons, the aforementioned transgenic models might be useful for devising clinical treatments in horses afflicted with sarcoid-related neoplasia of cutaneous and subcutaneous tissues.
Highlights
Sarcoid is one of the most common skin tumor types in equids
The switching on of procancerous mechanisms prompted by Rap1 signaling pathway and activation of proteoglycans is reflected in the presence of 49 and 48 Differentially Expressed Genes (DEGs), respectively. Crosstalk between these molecular regulatory networks in bovine papillomavirus (BPV)-E1ˆE4 transgenic equine adult cutaneous fibroblast cells (ACFCs)-derived neoplastic cells remains under control and requires the reciprocal cooperation of the panel of genes linked to Wnt signaling pathway and coding for such proteins as fibroblast growth factors, matrix metalloproteinases (MMPs), and interleukins (Table 4)
Crosstalk between these molecular regulatory networks in BPV-E1^E4 transgenic equine ACFC-derived neoplastic cells remains under control and requires the reciprocal cooperation of the panel of genes linked to Wnt signaling pathway and coding for such proteins as fibroblast growth factors, matrix metalloproteinases (MMPs), and interleukins (Table 4)
Summary
Sarcoid is one of the most common skin tumor types in equids. It does not belong to the metastasizing tumors but is considered to be locally invasive [1,2,3]. 2022, 23, 1970 tionally, the aforementioned strategies have been applied, for the first time, to research targeted at cell culture engineering and experimental and preclinical attempts, with the use of in vitro transgenic models designed to examine the molecular nature of sarcoid-dependent oncogenic transformation (carcinogenesis) of equine ACFCs. Sci. 2022, 23, 1970 tionally, the aforementioned strategies have been applied, for the first time, to research targeted at cell culture engineering and experimental and preclinical attempts, with the use of in vitro transgenic models designed to examine the molecular nature of sarcoid-dependent oncogenic transformation (carcinogenesis) of equine ACFCs These extracorporeal models have been developed to explore the genetic and epigenetic determinants of procancerous tumorigenesis of epidermal and dermal provenance in horses and phylogenetically consanguineous taxa (i.e., other equids). Our study sought to thoroughly unravel the modifications arising in genomic signatures that have incurred sarcoid-dependent alterations in transcriptomic profiles of horse ACFC-derived neoplastic cells
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