SNHG17 Serves as an Oncogenic lncRNA by Regulating the miR-361-3p/STC2 Axis in Rectal Cancer

Abstract

Long noncoding RNA (lncRNA) have been reported to be crucial regulators for carcinogenesis, including rectal cancer. This work aimed to explore the roles and associated mechanisms of small nucleolar RNA host gene 17 (SNHG17) in rectal cancer. A quantitative real-time polymerase chain reaction was performed to measure the expression level of SNHG17 in rectal cancer tissues and cells. Cell counting kit-8 (CCK-8) assay and flow cytometry assay were conducted to measure the biological roles of SNHG17 in rectal cancer. In addition, luciferase activity reporter assay, RNA immunoprecipitation (RIP) assay, and rescue experiments were conducted to explore the mechanisms of SNHG17 in rectal cancer. The upregulation status of SNHG17 was identified in rectal cancer tissues and cells. Functionally, knockdown the expression of SNHG17 inhibits rectal cancer cell proliferation via stimulating cell apoptosis. In vivo assay showed that the knockdown of SNHG17 inhibits tumor growth. Furthermore, we showed that microRNA-361-3p (miR-361-3p) has decreased expression in tumor tissues and cells, and SNHG17 functions as a sponge for miR-361-3p. The upregulation status of stanniocalcin 2 (STC2) was also found in rectal cancer, and the knockdown of STC2 hinders cancer progression. In conclusion, lncRNA SNHG17 functions as an oncogenic lncRNA in rectal cancer by regulating the miR-361-3p/STC2 axis.

Characterization of the Immune Infiltration Landscape and Identification of Prognostic Biomarkers for Esophageal Cancer

“…DKK1 overexpression in primary ESCA tumors was highly correlated with lymph node metastasis [22], which indicates a close relationship between DKK1 and the prognosis of patients with ESCA. Stanniocalcin 2 (STC2) is a homologue of a glycoprotein hormone and closely correlated with rectal cancer [23], lung cancer [24], and ovarian cancer [25]. STC2 is aberrantly expressed in ESCA with lymphatic metastasis and was verified to be an effective predictive marker for ESCA patients [26].…”

Enabling factor for cancer hallmark acquisition: Small nucleolar RNA host gene 17

“…Moreover, transcription factor yin-yang 1 (YY1) facilitates this upstream regulation of SNHG17 ( 33 ). Intriguingly, Wnt ligand secretion mediator (WLS) and stanniocalcin 2 (STC2) are involved in the pro-proliferative effects of SNHG17 as downstream targets ( 35 , 36 ), which are both closely related to the Wnt/β-catenin signaling pathway ( 37 , 38 ). However, additional research needs to verify whether SNHG17 can activate the Wnt/β-catenin pathway and thus promote tumor progression through WLS and STC2.…”

“…Moreover, transcription factor yin-yang 1 (YY1) facilitates this upstream regulation of SNHG17 (33). Intriguingly, Wnt ligand secretion mediator (WLS) and stanniocalcin 2 (STC2) are involved in the pro-proliferative effects of SNHG17 as downstream targets (35,36), which are both closely related to the Wnt/b-catenin signaling pathway (37, Schematic representation of the mechanisms by which SNHG17 plays in sustaining proliferative signaling. In the cytoplasm, SNHG17 acts as the ceRNA for miR-506-3 and miR-384 to activate the Wnt/b-catenin pathway and enhance the expression of CDK6 by targeting miR-214-3p.…”

­ Characterization of the Immune Infiltration Landscape and Identification of Prognostic Biomarkers for Esophageal Cancer

“…DKK1 overexpression in primary EC tumors was highly correlated with lymph node metastasis [20], which indicates a close relationship between DKK1 and the prognosis of patients with EC. Stanniocalcin 2 (STC2) is a homologue of a glycoprotein hormone and closely correlated with rectal cancer [21], lung cancer [22] and ovarian cancer [23]. STC2 is aberrantly expressed in EC with lymphatic metastasis and was veri ed to be an effective predictive marker for EC patients [24].…”