Aging-US: Characterization of LncRNA SNHG22 as a protector of NKIRAS211-10-2020
Aging-US recently published "Characterization of LncRNA SNHG22 as a protector of NKIRAS2 through miR-4492 binding in osteosarcoma\” which reported that the underlying mechanism of SNHG22 in regulating OS progression remains unknown.
In this study, the authors confirmed that SNHG22 was downregulated in OS, and the overexpression of SNHG22 significantly inhibited OS progression in vivo and in vitro.
Meanwhile, overexpression of SNHG22 also inhibited the migration and proliferation of human umbilical vein endothelial cells and prevented the epithelial-to-mesenchymal transition in OS.
Furthermore, the interaction between miR-4492 and SNHG22 they previously predicted was validated by RNA pull-down assays and RNA immunoprecipitation assays.
Dual-luciferase reporter assays showed that SNHG22 could directly interact with miR-4492 and upregulate the expression of NK-κB inhibitor-interacting Ras-like 2 by its competing endogenous RNA activity on miR-4492.
The Aging-US study has clarified the function of SNHG22 in OS progression and suggests a novel therapeutic target for OS.
Dr. Sheng-Dan Jiang and Dr. Lei-Sheng Jiang both from The Department of Clinic of Spine Center at Xinhua Hospital said, "Osteosarcoma (OS) is one of the most common primary malignant bone cancers in patients, which presents with two incidence peaks before older adulthood and frequently occurs in long bones such as distal femur and proximal tibia."
Therefore, it is important and urgent to develop new therapeutic targets for OS patients.
Recently, small nucleolar RNA host genes have become a focus of LncRNA research as potential therapeutic targets of cancer.
Figure 8. SNHG22 inhibited tumor growth in vivo. (A) HOS cells transfected with PLKO.1-VECTOR, PLKO.1-SNHG22, PLVX-VECTOR or PLVX-SNHG22 were inoculated into nude mice (n=5). The tumors were excised 3 weeks later. (B) Tumors from different groups were weighed. **P<0.01. (C) Tumor volumes were estimated (0.5 × width2 × length) by caliper every week. **P<0.01. (D) Proteins were extracted from tumors and the expression level of NKIRAS2 and PCNA was measured by western blot. (E) Schematic illustration of the role of SNHG22 in OS cells.
In this study, they investigated the impact of SNHG22 on OS and studied the underlying mechanisms. They found that SNHG22 was downregulated in lung metastatic sites compared with orthotopic OS.
Meanwhile, the authors revealed that SNHG22 could not only inhibited OS cell proliferation, migration and invasion, but also induced cell cycle arrest in vivo by sponging miR-4492 and acting as a competing endogenous RNA for NK-κB inhibitor-interacting Ras-like 2.
The research thus indicated that SNHG22 may be a promising therapeutic target in OS.
The Jiang/Jiang Research Team concluded in their Aging-US Research Paper, "we showed that SNHG22 was downregulated in OS compared with lung metastatic sites. We further found that SNHG22 induced cell cycle arrest in the G1 phase and inhibited the proliferation, migration and invasion of OS cells in vivo. This effect occurred mainly through the interaction with miR-4492, which subsequently targeted the transcription of NKIRAS2. SNHG22 also suppressed EMT in OS. In addition, SNHG22 inhibited the migration and proliferation of HUVECs, while SNHG22 silencing showed the opposite effect. Our study has thus demonstrated that SNHG22 was a pivotal regulator of OS and suggested that SNHG22 may be a novel target for treatment of OS."
Full Text - https://doi.org/10.18632/aging.103849
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.