Introduction:
SNHG3 (small nucleolar RNA host gene 3) is a long non-coding RNA (lncRNA) that plays a pivotal role in cellular regulation. It is intricately involved in modulating the cell cycle, enhancing cell proliferation, and inhibiting apoptosis. These functions position SNHG3 as a significant contributor to oncogenic processes. Given its substantial influence on tumorigenesis, elucidating the exact molecular mechanisms through which SNHG3 operates is paramount. Comprehensive understanding of SNHG3's interactions and pathways is not only critical for advancing our knowledge of cancer biology but also holds immense potential for identifying novel therapeutic targets. By targeting the regulatory networks associated with SNHG3, new strategies can be developed for the effective treatment of malignancies where SNHG3 is implicated.

Material and methods:
We investigated the role of lncRNA SNHG3 in promoting prostate cancer (PCa) proliferation and invasion. Using TCGA data, we assessed SNHG3 expression in cancer/adjacent tissue, Gleason score, biochemical recurrence, and overall survival. SNHG3 expression was manipulated in four cell types via siRNA interference/over-expression. Various experiments were conducted to confirm SNHG3's role in PCa, including clone ability, apoptosis, migration, Transwell invasion, and subcutaneous tumor experiments in nude mice.

Results:
In PCa, SNHG3 was highly expressed, especially in Gleason score >7 patients, correlating with shorter overall survival. Interfering with SNHG3 using a plasmid reduced proliferation, increased apoptosis, and decreased migration and tumor growth. Conversely, SNHG3 overexpression yielded opposite results.

Conclusions:
The lncRNA SNHG3 promotes PCa proliferation and invasion while inhibiting cell apoptosis.