<p>LncRNA SNHG7 Functions as an Oncogene in Cervical Cancer by Sponging miR-485-5p to Modulate JUND Expression</p>

Abstract

Background: Long non-coding RNA (LncRNA) SNHG7 is involved in the development of multiple cancers. However, its role in cervical cancer (CC) has not been elucidated. This study aimed to explore the function of SNHG7 in CC progression and the underlying mechanisms. Materials and Methods: The expression levels of SNHG7 and miR-485-5p in CC tissues and cell lines were measured by qPCR. Functional experiments including CCK-8 assay, wound healing assay, transwell assay, flow cytometry, Western blot, luciferases reporter assay and immunoprecipitation (RIP) were performed to explore the SNHG7/miR-485-5p/JUND pathway. Additionally, in vivo study was carried out by establishing tumor xenograft models. Results: We found that SNHG7 was markedly enhanced in CC tissues and cell lines, and associated with poor clinical characteristics. In vitro, knockdown of SNHG7 inhibited CC cell proliferation, migration and invasion, as well as aggravated cell apoptosis. As to mechanism investigation, rescue experiments revealed that miR-485-5p inhibitor could partially reverse the effects on CC cells induced by SNHG7 knockdown. SNHG7 upregulated JUND expression via miR-485-5p. Moreover, tumor xenograft models were established to confirm the findings in vivo. Conclusion: SNHG7 promoted CC progression through miR-485-5p/JUND axis. The SNHG7/miR-485-5p/JUND pathway might provide a novel therapeutic target for CC treatment.

RETRACTED ARTICLE: microRNA-375 released from extracellular vesicles of bone marrow mesenchymal stem cells exerts anti-oncogenic effects against cervical cancer

“…Our study further demonstrated that the BMSC-derived EVs could transfer miR-375 to cervical cancer cells and consequently acted as antioncogene in cervical cancer cells, evidenced by promoted cell apoptosis and inhibited cell migration and invasion. Importantly, the inhibited proliferation, migration, and invasion are significant indicators for the amelioration of cervical cancer [ 30 , 31 ]. Moreover, the present study clarified that BMSC-derived EV-incorporated miR-375 could ameliorate cervical cancer progression in vivo.…”

<p>Long Noncoding RNA <em>RGMB-AS1</em> Acts as a microRNA-574 Sponge Thereby Enhancing the Aggressiveness of Gastric Cancer via HDAC4 Upregulation</p>

“…Mechanistically, the most widely studied latent mechanism of action of lncRNAs is based on the role of a ceRNA that sponges miRNAs to alleviate the repression of their target genes. [30][31][32] Following the identification of the expression profile and functions of RGMB-AS1 in GC, it was necessary to elucidate the mechanisms responsible for the oncogenic activities of RGMB-AS1 in GC progression. Accordingly, we demonstrated that RGMB-AS1, which harbors miR-574-binding sites, can act as an effective sponge toward miR-574, thereby positively modulating HDAC4 expression.…”

Elevated microRNA‐130b‐5p or silenced ELK1 inhibits self‐renewal ability, proliferation, migration, and invasion abilities, and promotes apoptosis of cervical cancer stem cells

“…ELK1 expression was restrained by OE miR-330-5p and facilitated by knockdown of miR-330-5p. 15 Furthermore, ELK1 has a target relationship with miR-185-5p. 23 The most glamorous finding was that elevated miR-130b-5p or silenced ELK1 inhibited self-renewal ability, stemness, colony formation, proliferation, migration, and invasion abilities, promoted apoptosis of CC stem cells, and decreased the weight and volume of tumor in nude mice.…”

“…But there were no concrete studies about the relationship between miR‐130b‐5p and CC. ETS transcription factor (TF) (ELK1) is a transcription activator that regulates various genes regarding proliferation and metastasis 15 . A study has revealed that ELK1‐activated GPC3‐AS1/GPC3 axis is beneficial for the progress of CC cells 16 .…”

“…ETS transcription factor (TF) (ELK1) is a transcription activator that regulates various genes regarding proliferation and metastasis. 15 A study has revealed that ELK1-activated GPC3-AS1/GPC3 axis is beneficial for the progress of CC cells. 16 Without the specific literatures about the relationship between miR-130b-5p, ELK1, and CC, this study explored the role of miR-130b-5p in self-renewal ability and stemness of CC stem cells by targeting ELK1.…”