癌肿块由异质细胞群组成，其中一小部分构成癌症干细胞，因为它们分化程度较低且具有较高的发展癌症的能力。 Versican 是一种存在于许多人体组织中的细胞外基质蛋白。通过 RT-PCR、Northern 印迹分析和 cDNA 测序检测发现，多功能蛋白聚糖的 mRNA 具有“剪接模式”。基于这一知识，本研究旨在揭示多功能蛋白聚糖分子的剪接变体，这些剪接变体被认为参与DU-145人前列腺癌细胞系和从该细胞系分离的前列腺癌干细胞的发病机制。在本研究中，使用了RWPE-1正常前列腺细胞系和DU-145人类前列腺癌细胞系。根据其 CD133 /CD44 分离前列腺癌干细胞和其余组的非前列腺癌干细胞（群体）。分离所有组中的RNA，并通过Illumina NextSeq 500测序系统完成剪接变体的序列分析。通过生物信息学评估对结果进行分析。通过分析 Versacan 基因的 5 个异构体在差异转录表达中的情况，观察到仅在异构体 Versican 0 和 Versican 1 中发现显着变化。在本研究中，我们探讨了该分子的功能，我们认为该分子是对癌症进展有效，并表明完成体内实验后可以获得更有价值的结果。版权所有 © 2024 Elsevier GmbH。版权所有。

A cancer mass is composed of a heterogeneous group of cells, a small part of which constitutes the cancer stem cells since they are less differentiated and have a high capacity to develop cancer. Versican is an extracellular matrix protein located in many human tissues. The mRNA of versican has been shown to have "splicing patterns" as detected by RT-PCR, northern blot analysis, and cDNA sequencing. Based on this knowledge this study aims to reveal the splice variants of versican molecules, which are thought to be involved in the pathogenesis of the DU-145 human prostatic carcinoma cell line and prostatic cancer stem cells isolated from this cell line. In this study, RWPE-1 normal prostatic and DU-145 human prostate cancer cell lines have been used. Prostatic cancer stem cells and the remaining group of non-prostatic-cancer stem cells (bulk population) were isolated according to their CD133+/CD44+. RNA was isolated in all groups, and sequence analysis was accomplished for splicing variants by Illumina NextSeq 500 sequencing system. The results were analyzed by bioinformatic evaluation. As five isoforms of the versican gene in the differential transcript expression are analyzed, it was observed that a significant change was only found in the isoforms Versican 0 and Versican 1. In this study, we explored the function of this molecule which we think to be effective in cancer progression, and suggested that more valuable results can be obtained after the accomplishment of in vivo experiments.Copyright © 2024 Elsevier GmbH. All rights reserved.