<p>Long Noncoding RNA SNHG7, a Molecular Sponge for microRNA-485, Promotes the Aggressive Behavior of Cervical Cancer by Regulating PAK4</p>

Abstract

Purpose: A long noncoding RNA called small nucleolar RNA host gene 7 (SNHG7) is known to be a key regulator of biological processes in multiple human cancer types. In this study, our aims were to determine the expression status of SNHG7 in cervical cancer, to figure out the detailed roles of SNHG7 in cervical cancer cells, and to identify the mechanism underlying the activity of SNHG7 in cervical cancer. Methods: Reverse-transcription quantitative PCR was performed to measure SNHG7 expression in cervical cancer. A Cell Counting Kit-8 assay, flow-cytometric analysis, cell migration and invasion assays, and a tumor xenograft experiment were conducted to respectively determine the effects of SNHG7 on cervical cancer cell proliferation, apoptosis, migration, and invasion in vitro and tumor growth in vivo. Results: SNHG7 was found to be markedly upregulated in cervical cancer tissues and cell lines. Higher SNHG7 expression significantly correlated with FIGO stage, lymph node metastasis, the depth of cervical invasion, and shorter overall survival in patients with cervical cancer. Functional experiments indicated that a SNHG7 knockdown attenuated proliferation, migration, and invasiveness and promoted apoptosis of cervical cancer cells in vitro. The SNHG7 knockdown also slowed tumor growth in vivo. Further investigation showed that SNHG7 acts as a competing endogenous RNA for microRNA-485 (miR-485) in cervical cancer cells, and the inhibitory actions of the SNHG7 knockdown on the malignant phenotype were reversed by miR-485 inhibition. P21-activated kinase 4 (PAK4) was identified as a direct target gene of miR-485 in cervical cancer, and PAK4 expression was promoted by SNHG7. Conclusion: SNHG7 functions as an oncogenic RNA in cervical cancer, competitively binds to miR-485, and thereby upregulates PAK4. This SNHG7-miR-485-PAK4 regulatory network may provide insights into the pathogenesis of cervical cancer, and can help in the identification of novel diagnostic and therapeutic approaches for cervical cancer.

A novel mechanism by which ACTA2-AS1 promotes cervical cancer progression: acting as a ceRNA of miR-143-3p to regulate SMAD3 expression

“…LncRNAs can affect various aspects of cellular homeostasis, including cell proliferation, migration, apoptosis or genomic stability [7]. According to previous studies, some lncRNAs could play a crucial role in the progression of CC, such as GHET1 [8], SNHG7 [9] and WT1-AS [10]. In our previous RNA-sequencing analysis (unpublished data), we found that lncRNA ACTA2 antisense RNA 1 (ACTA2-AS1) showed significant higher expression in CC tissues compared to adjacent normal tissues (ANT).…”

Long Non-Coding RNA LINC00313 Accelerates Cervical Carcinoma Progression by miR-4677-3p/CDK6 Axis

“… 4 Increasing articles have reported that lncRNAs regulate the expression of downstream genes, and then participate in the occurrence and development of tumors. 5–7 For example, the up-regulation of lncRNA MALAT1 in cervical carcinoma tissues significantly affects the tumor size, TNM stage, and lymph node metastasis. 8 , 9 Also, the negative regulation of GAS5 in cervical carcinoma was also significantly correlated with the progression.…”

Prenatal cadmium exposure alters proliferation in mouse CD4+ T cells via LncRNA Snhg7

“…We further demonstrate that prenatal Cd exposure exacerbates this phenotype resulting in aberrant T cell proliferation. Several reports in various cancer cells demonstrate that lncSnhg7 regulates cellular proliferation through a variety of signaling pathways (22,27,31,32,(51)(52)(53)(54)(55). While there are many mechanisms by which lncSnhg7 promotes cell proliferation in cancer, a main feature is its ability to sponge microRNAs promoting the upregulation of downstream signaling proteins.…”