LncRNA SNHG16 promotes development of oesophageal squamous cell carcinoma by interacting with EIF4A3 and modulating RhoU mRNA stability

Ren, Lihua; Fang, Xin Jian; Shrestha, Sachin Mulmi; Ji, Qinghua; Ye, Hui; Liang, Yan; Liu, Yang; Feng, Yadong; Dong, Jingwu; Shi, Ruihua

doi:10.1186/s11658-022-00386-w

Cited by 25 publications

(17 citation statements)

References 47 publications

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“…A previous study has reported that LncRNA Tug1 regulates the bioenergetic environment of patients with mitochondrial diabetic nephropathy [ 21 ]. Currently, SNHG16 is considered as an oncogene in many cancers [ 23 , 24 ]. However, it has been less studied in diabetes.…”

Section: Discussionmentioning

confidence: 99%

Silencing LncRNA SNHG16 suppresses the diabetic inflammatory response by targeting the miR-212-3p/NF-κB signaling pathway

Huang

Xiong

Liu

et al. 2023

Diabetol Metab Syndr

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Background Long noncoding RNAs (LncRNAs) have been identified to play an important role in diabetes. The aim of the present study was to determine the expression and function of small nucleolar RNA host gene 16 (SNHG16) in diabetic inflammation. Methods For the in vitro experiments, quantitative real-time PCR (qRT-PCR), Western blotting and immunofluorescence were used to detect LncRNA SNHG16 expression in the high-glucose state. The potential microRNA sponge target of LncRNA SNHG16, miR-212-3p, was detected by dual-luciferase reporter analysis and qRT-PCR. For the in vivo experiments, glucose changes in mice were detected after si-SNHG16 treatment, and SNHG16 and inflammatory factor expression in kidney tissues were detected by qRT-PCR and immunohistochemistry. Results LncRNA SNHG16 was upregulated in diabetic patients, HG-induced THP-1 cells, and diabetic mice. Silencing SNHG16 inhibited the diabetic inflammatory response and the development of diabetic nephropathy. miR-212-3p was found to be directly dependent on LncRNA SNHG16. miR-212-3p could inhibitor P65 phosphorylation in THP-1 cells. The miR-212-3p inhibitor reversed the action of si-SNHG16 in THP-1 cells and induced an inflammatory response in THP-1 cells. LncRNA SNHG16 was also found to be higher in the peripheral blood of diabetic patients than in the normal person. The area under the ROC curve is 0.813. Conclusion These data suggested that silencing LncRNA SNHG16 suppresses diabetic inflammatory responses by competitively binding miR-212-3p to regulate NF-κB. LncRNA SNHG16 can be used as a novel biomarker for patients with type 2 diabetes.

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Section: Discussionmentioning

confidence: 99%

Silencing LncRNA SNHG16 suppresses the diabetic inflammatory response by targeting the miR-212-3p/NF-κB signaling pathway

Huang

Xiong

Liu

et al. 2023

Diabetol Metab Syndr

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“…In addition, eukaryotic translation initiation factor 4A3 (EIF4A3) is a member of RBPs, which is able to act as an oncogene in ESCA (13). For instance, lncRNA SNHG16 was able to promote the development of ESCA by interacting with EIF4A3 (14). In this study, the prediction of starbase indicated SSTR5-AS1 might interact with EIF4A3, while the detailed relation between SSTR5-AS1 and EIF4A3 remains largely unknown.…”

Section: Introductionmentioning

confidence: 87%

LncRNA SSTR5-AS1 promotes esophageal carcinoma through regulating ITGB6/JAK1/STAT3 signaling

Tang,

Jiang,

Zong

et al. 2023

Preprint

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Background Esophageal carcinoma (ESCA) is the aggressive cancer which threatens people’s health. LncRNA SSTR5-AS1 is upregulated in ESCA. However, the potential regulatory mechanism of SSTR5-AS1 in ESCA is unknown. Methods GEPIA was used to explore the prognosis of SSTR5-AS1 in ESCA patients. EdU staining was used to detect cell proliferation. Transwell assay was applied for assessing cell invasion and migration. Meanwhile, RNA pull-down and RIP were applied to assess the relationship among SSTR5-AS1, EIF4A3 and ITGB6, and FISH was applied for exploring the localization of SSTR5-AS1 in ESCA cells. Results SSTR5-AS1 was upregulated in ESCA. SSTR5-AS1 downregulation repressed the invasion and migration of ESCA cells, and promoted cells apoptosis. Furthermore, SSTR5-AS1 shRNA upregulated the levels of Bax, cleaved caspase 3 and inhibited p-STAT3, p-JAK1 and Bcl-2 levels. SSTR5-AS1 was distributed in cytoplasm, and it could regulate ITGB6 by interacting with EIF4A3. SSTR5-AS1 silencing inhibited ITGB6 expression and inactivated JAK1/STAT3 signaling, while EIF4A3 upregulation reversed this phenomenon. In addition, SSTR5-AS1 silencing attenuated the malignant behavior of ESCA cells through ITGB6-mediated JAK1/STAT3 signaling. Conclusion SSTR5-AS1 promotes ESCA development through interacting with EIF4A3 to regulate ITGB6/JAK1/STAT3 signaling. Hence, this research supplied a basis for discovering strategies against ESCA.

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“…As reported, circRNAs regulate the biological activity of downstream targets by binding to RBPs [ 15 ]. EIF4A3 is a commonly studied RBP involved in posttranscriptional regulation [ 16 , 17 ]. For example, EIF4A3 interacts with circ_0084615, promoting progression of colorectal cancer via miR-599/ONECUT2 [ 18 ].…”

Section: Introductionmentioning

confidence: 99%

Hsa_circ_0005397 promotes hepatocellular carcinoma progression through EIF4A3

Yuan,

Luo,

Liu

et al. 2024

BMC Cancer

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Purpose The purpose of this study was to explore the expression and potential mechanism of hsa_circ_0005397 in hepatocellular carcinoma progression. Methods Quantitative reverse transcription-polymerase chain reaction(qRT-PCR) was used to measure the expression level of hsa_circ_0005397 and EIF4A3 from paired HCC tissues and cell lines. Western Blot (WB) and immunohistochemistry (IHC) were used to verify the protein level of EIF4A3. The specificity of primers was confirmed by agarose gel electrophoresis. Receiver Operating Characteristic (ROC) Curve was drawn to analyze diagnostic value. Actinomycin D and nuclear and cytoplasmic extraction assays were utilized to evaluate the characteristics of hsa_circ_0005397. Cell Counting kit-8 (CCK-8) and colony formation assays were performed to detect cell proliferation. Flow cytometry analysis was used to detect the cell cycle. Transwell assay was performed to determine migration and invasion ability. RNA-binding proteins (RBPs) of hsa_circ_0005397 in HCC were explored using bioinformatics websites. The relationship between hsa_circ_0005397 and Eukaryotic Translation Initiation Factor 4A3 (EIF4A3) was verified by RNA Binding Protein Immunoprecipitation (RIP) assays, correlation and rescue experiments. Results In this study, hsa_circ_0005397 was found to be significantly upregulated in HCC, and the good diagnostic sensitivity and specificity shown a potential diagnostic capability. Upregulated expression of hsa_circ_0005397 was significantly related to tumor size and stage. Hsa_circ_0005397 was circular structure which more stable than liner mRNA, and mostly distributed in the cytoplasm. Upregulation of hsa_circ_0005397 generally resulted in stronger proliferative ability, clonality, and metastatic potency of HCC cells; its downregulation yielded the opposite results. EIF4A3 is an RNA-binding protein of hsa_circ_0005397, which overexpressed in paired HCC tissues and cell lines. In addition, expression of hsa_circ_0005397 decreased equally when EIF4A3 was depleted. RIP assays and correlation assay estimated that EIF4A3 could interacted with hsa_circ_0005397. Knockdown of EIF4A3 could reverse hsa_circ_0005397 function in HCC progression. Conclusions Hsa_circ_0005397 promotes progression of hepatocellular carcinoma through EIF4A3. These research findings may provide novel clinical value for hepatocellular carcinoma.

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LncRNA SNHG16 promotes development of oesophageal squamous cell carcinoma by interacting with EIF4A3 and modulating RhoU mRNA stability

Cited by 25 publications

References 47 publications

Silencing LncRNA SNHG16 suppresses the diabetic inflammatory response by targeting the miR-212-3p/NF-κB signaling pathway

Silencing LncRNA SNHG16 suppresses the diabetic inflammatory response by targeting the miR-212-3p/NF-κB signaling pathway

LncRNA SSTR5-AS1 promotes esophageal carcinoma through regulating ITGB6/JAK1/STAT3 signaling

Hsa_circ_0005397 promotes hepatocellular carcinoma progression through EIF4A3

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