SPIN.DOC诱导NIH3T3正常小鼠成纤维细胞发生细胞转化。

SPIN.DOC induces cellular transformation of NIH3T3 normal mouse fibroblast cells.

作者信息

Devi Khuraijam Mrinalini, Singh Thangjam Davis, Deka Rubismita, Singh Lisam Shanjukumar, Singh Thiyam Ramsing

机构信息

Department of Biotechnology, Manipur University, Imphal -795003, India.

Department of Molecular Biology and Biotechnology, Tezpur University, Napaam, Tezpur 784028, Assam, India.

出版信息

Mol Biol Res Commun. 2025;14(4):283-289. doi: 10.22099/mbrc.2025.52821.2125.

DOI:10.22099/mbrc.2025.52821.2125

PMID:40949799

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12426960/

Abstract

SPIN.DOC was discovered as a transcriptional co-repressor of wingless related integration site (WNT) pathway. However, it has been found to be upregulated in various types of cancer, including hepatocellular carcinoma, colorectal cancer, renal papillary cell carcinoma. Whether SPIN.DOC functions as an oncogene or tumour suppressor gene remains uncertain. Here, we report that ectopic expression of SPIN.DOC in normal NIH3T3 fibroblast cells promotes cell proliferation, colony formation, migration and invasion. Moreover, SPIN.DOC expressing NIH3T3 cells show increased spheroid formation, suggesting enhanced stemness and transformation potential. Immunofluorescence analysis using anti-β-Tubulin suggests that SPIN.DOC may induce, formation of tubulin-based microtentacles (McTNs), indicating epithelial-to-mesenchymal (EMT) transition. In conclusion, our study helps in establishing that SPIN.DOC can function as an oncogene.

摘要

SPIN.DOC被发现是无翅相关整合位点（WNT）信号通路的转录共抑制因子。然而，现已发现它在包括肝细胞癌、结直肠癌、肾乳头状细胞癌在内的多种癌症中上调。SPIN.DOC是作为癌基因还是肿瘤抑制基因发挥作用仍不确定。在此，我们报告在正常NIH3T3成纤维细胞中异位表达SPIN.DOC可促进细胞增殖、集落形成、迁移和侵袭。此外，表达SPIN.DOC的NIH3T3细胞显示出更强的球体形成能力，表明其干性和转化潜能增强。使用抗β-微管蛋白的免疫荧光分析表明，SPIN.DOC可能诱导基于微管蛋白的微触手（McTNs）形成，提示上皮-间质转化（EMT）。总之，我们的研究有助于确定SPIN.DOC可作为癌基因发挥作用。