Expression and functional characterization of lncRNA SNHG4 in colorectal cancer
Year: 2026
Type: article
Abstract: Long noncoding RNA SNHG4 has been implicated in colorectal cancer (CRC), but its expression across independent clinical cohorts and its contribution to CRC-related cellular phenotypes remain incompletely understood. SNHG4 expression was evaluated in GSE87211, TCGA-READ, TCGA-COAD, and paired specimens from a local CRC cohort. Clinicopathological associations were explored, and the effects of SNHG4 depletion were examined in HT29 and SW620 cells and in a subcutaneous xenograft model. Changes in miR-125a-3p and IGF2 expression were measured after RNA manipulation. Luciferase reporter assays assessed sequence responsiveness, and rescue experiments examined whether miR-125a-3p and IGF2 contributed to the phenotypes observed after SNHG4 depletion. SNHG4 expression was higher in rectal tumors in GSE87211 and TCGA-READ, in colon tumors in TCGA-COAD, and in local paired CRC specimens. In the local cohort, high SNHG4 expression was associated with larger tumor diameter and lymph-node metastasis in exploratory univariable analyses. SNHG4 depletion reduced CRC-cell viability, colony formation, wound closure, Transwell migration and invasion, and subcutaneous xenograft growth. SNHG4 and miR-125a-3p showed reciprocal expression changes and sequence-dependent reporter responses. IGF2 responded to miR-125a-3p, and IGF2 silencing attenuated the phenotypic rescue produced by miR-125a-3p inhibition in SNHG4-depleted cells. SNHG4 was consistently elevated in the CRC cohorts examined and was associated with growth- and motility-related phenotypes in CRC models. The reporter and rescue findings further identify miR-125a-3p and IGF2 as plausible contributors to these SNHG4-associated effects. Together, the data support SNHG4 as a candidate regulator of CRC-related phenotypes and provide a basis for further mechanistic investigation.
Source: Discover Oncology
Authors: Shanshan Feng, Yanbai Wang, Tao Jiang, Zhenhui Lu
Language: English
Subfield: Cancer Research
Domain: Life Sciences
Open Access status: gold
Estimated APC paid: $1,690
OpenAlex ID: W7225651996
FWCI:
Cites:
Cited by:
Related to:
