C57BL/6JCya-Snhg1^em1/Cya

Snhg1, short for Small nucleolar RNA host gene 1, is an important member of the SNHG family. This family consists of host genes that can be processed into small nucleolar RNAs and perform significant biological functions. Snhg1, as a long non-coding RNA (lncRNA), is involved in various cellular processes. It has been found to be associated with pathways related to tumorigenesis, cell proliferation, metastasis, and immune cell interaction [1,3,4,5,6,7,8,9,10].

In multiple cancers, Snhg1 shows oncogenic properties. For instance, in breast cancer, knockdown of Snhg1 in macrophages inhibited M2 macrophage polarization by suppressing STAT6 phosphorylation, alleviating MCF-7 cell migration and tube formation of HUVEC, thus reversing the promotion of tumor growth and angiogenesis [2]. In colorectal cancer, Snhg1 knockdown repressed cell growth both in vitro and in vivo. Mechanistically, in the nucleus, it interacted with PRC2 to modulate histone methylation of KLF2 and CDKN2B promoters, and in the cytoplasm, it sponged miR-154-5p to upregulate CCND2 expression [4]. Also, in metastatic colorectal cancer, Snhg1 promoted cell migration and invasion by recruiting HNRNPD to stabilize SERPINA3 mRNA [5]. In neuroblastoma, disrupting endogenous Snhg1 using CRISPR/Cas9 suppressed cell proliferation and colony formation ability, and affected the expression of core regulatory circuitry transcription factors, potentially due to interactions between Snhg1 and HDAC1/2 [6].

In conclusion, Snhg1 plays crucial roles in tumor-related biological processes. The findings from loss-of-function experiments, such as knockdown in various cancer cell lines, reveal its oncogenic function in promoting cancer cell growth, metastasis, and in modulating immune-tumor cell interactions. These studies contribute to understanding the mechanisms of cancer development and suggest Snhg1 as a potential biomarker and therapeutic target in cancer [1,2,3,4,5,6,7,8,9,10].