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Research Paper Volume 12, Issue 5 pp 4527-4546
LncRNA-LALR1 upregulates small nucleolar RNA SNORD72 to promote growth and invasion of hepatocellular carcinoma
Relevance score: 12.472574Lin-Hong Mao, Si-Yuan Chen, Xiao-Qin Li, Feng Xu, Jing Lei, Qing-Liang Wang, Li-Yang Luo, Hai-Yan Cao, Xin Ge, Tao Ran, Xue Li, Min Zou, Zhi-Hang Zhou, Xiao-Ling Wu, Song He
Keywords: lncRNA-LALR1, SNORD72, ID2, HCC, mRNA stability
Published in Aging on March 11, 2020
LncRNA-LALR1 is highly expressed in HCC samples. (A) qRT-PCR assay showing the expression of lncRNA-LALR1 in HCC tissues and matched non-tumor tissues. (B) The expression of lncRNA-LALR1 in tumor samples from HCC patients with distant metastasis. (C) The expression of lncRNA-LALR1 in tumor samples from HCC patients with poor differentiation (D) qRT-PCR assay showing the expression of lncRNA-LALR1 in six HCC cell lines. (E) Fluorescence in situ hybridization (FISH) assay showing the localization of lncRNA-LALR1 in HCC cells. *: P < 0.05.
Knock-down of lncRNA-LALR1 suppresses growth and invasion of HCC cells in vitro. (A) CCK-8 assay showing knockdown of lncRNA-LALR1 decreases the proliferation ability compared with control group of SMMC-7721 cells. (B) Colony formation assay showing lncRNA-LALR1 knockdown reduces the growth ability compared with control group of SMMC-7721 cells. (C) Colony formation assay showing lncRNA-LALR1 knockdown reduces the growth ability compared with control group of SMMC-7721 cells. (D) CCK-8 assay showing knockdown of lncRNA-LALR1 decreases the proliferation ability compared with control group of HepG2 cells. (E) Colony formation assay showing lncRNA-LALR1 knockdown reduces the growth ability compared with control group of HepG2 cells. (F) Colony formation assay showing lncRNA-LALR1 knockdown reduces the growth ability compared with control group of HepG2 cells. (G) Western Blot assay showing knockdown of lncRNA-LALR1 downregulates cyclinD1, cyclinE1, MMP-2 and MMP-9. (H) Transwell invasion assay showing lncRNA-LALR1 silencing decreases the invasion ability compared with control group of SMMC-7721 cells. (I) Transwell invasion assay showing lncRNA-LALR1 silencing decreases the invasion ability compared with control group of HepG2 cells. *: P < 0.05; **: P < 0.01; ***: P < 0.001.
Knock-down of lncRNA-LALR1 inhibits growth of HCC cells in vivo. (A) The tumor volumes after knockdown of lncRNA-LALR1. (B) Knockdown of lncRNA-LALR1 decreases tumor volumes. (C) Knockdown of lncRNA-LALR1 decreases tumor weights. (D) Immunohistochemistry showing lncRNA-LALR1 silencing leads to a reduce of Ki67 protein levels. (E) LncRNA-LALR1 silencing reduces Ki67 protein levels. *: P < 0.05; **: P < 0.01; ***: P < 0.001.
GO and KEGG analysis of differentially expressed genes after knockdown of lncRNA-LALR1. (A) Cellular component analysis of the differentially expressed genes. (B) Cellular process analysis of the differentially expressed genes. (C) KEGG signaling analysis of the differentially expressed genes.
LncRNA-LALR1 upregulates SNORD72 and ID2 in HCC cells. (A) qRT-PCR showing the expression of SNORD72 and ID2 after lncRNA-LALR1 silencing in SMMC-7721 cells. (B) Western blot showing the expression of ID2 after lncRNA-LALR1 silencing in SMMC-7721 cells. (C) qRT-PCR showing the expression of SNORD72 and ID2 after knockdown of lncRNA-LALR1 in HepG2 cells. (D) Western blot showing the expression of ID2 after lncRNA-LALR1 silencing in HepG2 cells. (E) FISH assay showing the expression of SNORD72 after lncRNA-LALR1 silencing in SMMC-7721 cells. (F) FISH assay showing the expression of ID2 after lncRNA-LALR1 silencing in SMMC-7721 cells. (G) FISH showing lncRNA-LALR1 is co-localized with SNORD72 in HepG2, SMMC-7721, PLC/PRF/5, Sk-Hep1 cells. (H) RNA pulldown assay showing lncRNA-LALR1 interacts with SNORD72 and ID2 mRNA. (I) The effect of lncRNA-LALR1 on the mRNA stability of ID2. (J) The effect of lncRNA-LALR1 on the mRNA stability of SNORD72. *: P < 0.05; **: P < 0.01; ***: P < 0.001; ns: no significant.
SNORD72 is upregulated in HCC samples and promotes proliferation and invasion of HCC cells. (A) Bioinformatic analysis showing the expression of SNORD72 in HCC tissues and adjacent non-tumor tissues. (B) qRT-PCR assay showing the expression of SNORD72 in HCC tissues and matched non-tumor tissues. (C) Bioinformatic analysis showing the relationship between SNORD72 expression and the differentiation degree. (D) qRT-PCR assay verifying the overexpression of SNORD72. (E) FISH assay verifying the overexpression of SNORD72. (F) CCK-8 assay showing overexpression of SNORD72 increases the proliferation ability compared with control group in vitro. (G) Colony formation assay showing overexpression of SNORD72 increases the growth ability compared with control group in vitro. (H) Transwell invasion assay showing overexpression of SNORD72 increases the invasion ability compared with control group in vitro. (I) qRT-PCR assay showing the effect of SNORD72 on the expression of ID2. (J) Western blot assay showing the effect of SNORD72 on the expression of ID2. (K) FISH assay showing the effect of SNORD72 on the expression of ID2. (L) The effect of SNORD72 on the mRNA stability of ID2. *: P < 0.05; **: P < 0.01; ***: P < 0.001.
Overexpression of SNORD72 restored the proliferation, colony formation and invasion capacity in lncRNA-LALR1-knockdown cells. (A) qRT-PCR assay showing the overexpression of SNORD72 in lncRNA-LALR1-knockdown cells. (B) CCK-8 assay showing overexpression of SNORD72 rescues the proliferation ability compared with control group in vitro. (C) Colony formation assay showing overexpression of SNORD72 rescues the growth ability compared with control group in vitro. (D) Colony formation assay showing overexpression of SNORD72 rescues the growth ability compared with control group. (E) Transwell invasion assay showing overexpression of SNORD72 rescues the invasion ability compared with control group in vitro. (F) Transwell invasion assay showing overexpression of SNORD72 rescues the invasion ability compared with control group. *: P < 0.05; **: P < 0.01; ***: P < 0.001.
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Editorial Volume 10, Issue 11 pp 3046-3047
Cardiovascular disease, inflammation, and mRNA stability
Relevance score: 11.190653Allison B. Herman, Michael V. Autieri
Keywords: mRNA stability, vascular smooth muscle cells, interleukin-19, FXR1
Published in Aging on October 26, 2018
Proposed working hypothesis of IL-19 reduction of inflammatory mRNA stability. Under inflammatory conditions, HuR interacts with ARE in pro-inflammatory and HuR mRNA 3’UTR and stabilizes the transcript, resulting in increased inflammatory protein abundance. When inflammation is reduced, FXR1 expression increases, with the dual outcome of increased competition with HuR for ARE occupancy, as well as reduced HuR abundance. This results in reduced transcript stability.
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Research Paper Volume 4, Issue 10 pp 695-708
NF90 coordinately represses the senescence-associated secretory phenotype
Relevance score: 10.299577Kumiko Tominaga-Yamanaka, Kotb Abdelmohsen, Jennifer L. Martindale, Xiaoling Yang, Dennis D. Taub, Myriam Gorospe
Keywords: RNA-binding protein, ribonucleoprotein complex, mRNA translation, mRNA stability, post-transcriptional gene regulation, senescence
Published in Aging on October 31, 2012
(A) Western blot analysis of the expression levels of RBPs HuR, AUF1, NCL and NF90 in whole-cell lysates prepared from human diploid WI-38 fibroblasts ['young', proliferating (P, pdl 20) or senescent (S, pdl 54)] and from human IDH4 fibroblasts [P (+Dex) or S (-Dex for 9 days)]; the levels of GAPDH were assessed as a loading control. (B) Western blot analysis of the senescence-associated cdk inhibitor p21 in cells from the populations described in panel A. (C,D) In the WI-38 (C) and IDH4 (D) cell populations described in panel A, total RNA was prepared and the levels of mRNAs encoding the SASP factors shown were measured by RT-qPCR. Data are the means and standard deviation (+SD) from three independent experiments.
(A) Lysates were prepared from proliferating WI-38 (P) and IDH4 (+Dex) cells and subjected to immunoprecipitation (IP) using either anti-NF90 or IgG antibodies, whereupon Western blot (WB) analysis was used to detect NF90 levels in the IP samples. (B,C) The levels of SASP mRNAs in the ribonucleoprotein (RNP) complexes present in the IgG IP and NF90 IP samples from panel A were measured by RT-qPCR analysis. The levels of enrichment of SASP mRNAs in NF90 IP relative to IgG IP were calculated. Enrichments >2-fold are shown for WI-38 cells (B) and enrichments >1.5-fold are shown for IDH4 cells (C). In (B,C) data are the means +SD from three independent experiments.
(A) Forty-eight h after transfecting WI-38 cells (pdl 30) and IDH4 cells (+Dex) with either NF90 siRNA or Ctrl siRNA, whole-cell lysates were prepared and the levels of senescence markers p21, p53, and p16 were studied by Western blot analysis. (B) WI-38 and IDH4 cells were transfected as explained in panel A; two weeks later cells were counted and plotted. Data represent the means +SD from three independent experiments.
(A) Forty-eight h after transfecting WI-38 cells (pdl 30) with Ctrl siRNA or NF90 siRNA, total RNA was prepared and the levels of SASP mRNAs were quantified by RT-qPCR analysis (normalized to 18S rRNA levels). (B) Forty-eight h after transfecting IDH4 cells (+Dex) with Ctrl siRNA or NF90 siRNA, total RNA was prepared and the levels of SASP mRNAs were quantified by RT-qPCR analysis (normalized to 18S rRNA levels). Data represent the means +SD from three independent experiments.
(A) Schematic of reporters used. Reporter constructs were derived from the psiCHECK2 parent plasmid by insertion of 3'UTRs from CCL2, CCL16, TNFRSF11B, CSF2, CXCL1, IL8, and IL6 mRNAs (gray) in the 3' end of the renilla luciferase (RL) coding region (dark blue); the internal transfection control firefly luciferase (FL, light blue) was expressed from the same plasmid backbone. (B) Biotin pulldown analysis of the interaction of NF90 with the biotinylated 3'UTRs shown in panel A (gray) was carried out as explained in the Methods section. Negative control RNAs spanned the 5'UTR and CR of the nucleolin (NCL) mRNA. (C)Left, WI-38 cells (pdl 30) were transfected with Ctrl or NF90 siRNAs; 24 h later, cells were further transfected with each of the plasmids shown [WI-38 cells (800 ng/ml plasmid) and IDH4 cells (8 ng/ml plasmid)] and 16 h after that, the levels of Renilla luciferase were calculated and normalized to the levels of Firefly luciferase in the same transfection group. Right, the “translation indeces” were calculated for the reporter constructs. Relative differences in RL/FL were compared with differences in RL mRNA/FL mRNA, in order to calculate how much of the changes in reporter activity were due to changes in transcript levels (relative to changes in protein levels). (D) IDH4 cells were transfected and investigated using the same strategies as described in panel C. In (C,D) data are the means +SD from three independent experiments.
(A) The levels of the SASP factors shown (GM-CSF, MCP-1, GROa, IL-6, and IL-8) were measured in supernatants from cultures of WI-38 cells (P, pdl 20; S, pdl 54) and IDH4 cells (+Dex, -Dex for 9 days). (B) The levels of the SASP factors were measured in supernatants from cultures of WI-38 cells (pdl 30) and IDH4 cells (+Dex) that were transfected with Ctrl siRNA or NF90 siRNA. SASP factor levels were studied 1–3 weeks after transfection of WI-38 cells (top) and 1 and 2 week after transfection of IDH4 cells (bottom). In (A,B), data represent the means +SD from 3 independent experiments.