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• Research Paper Volume 13, Issue 19 pp 22963-22984

  RUNX2 and LAMC2: promising pancreatic cancer biomarkers identified by an integrative data mining of pancreatic adenocarcinoma tissues

  Relevance score: 7.7270274

  Guihua Jin, Qingqing Ruan, Fugen Shangguan, Linhua Lan

  Keywords: pancreatic carcinoma, bioinformatics analysis, biomarkers, LAMC2, RUNX2

  Published in Aging on October 4, 2021

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  Pancreatic carcinoma (PC) is a severe disease associated with high mortality. Although strategies for cancer therapy have made great progress, outcomes of pancreatic carcinoma patients remain extremely poor. Therefore, it is urgent to find novel biomarkers and therapeutic targets. To identify biomarkers for early diagnosis and therapy, three mRNA microarray datasets and two miRNA datasets were selected, and combinative analysis was performed by GEO2R. Functional and pathway enrichment analysis were performed using DAVID database. MiRTarBase, miRWalk and Diana Tools were used to get key genes. TCGA, HPA and western blotting were used to verify diagnostic and prognostic value of key genes. By integrating mRNA and miRNA expression profiles, we identified 114 differentially expressed genes and 114 differentially expressed miRNAs, respectively. Then, three overlapping key genes, RUNX2, LAMC2 and FBXO32, were found. Their protein levels in pancreatic tissue from PC patients and normal people were analyzed by immunohistochemical staining and western blotting. RUNX2 showed a potential property to identify PC. Aberrant over-expression of LAMC2 was associated with poor prognosis of PC patients, tumor status and subtypes. In summary, our current study identified that RUNX2 and LAMC2 may be promising targets for early diagnosis and therapy of PC patients.

• Research Paper Volume 12, Issue 12 pp 11623-11635

  Silencing of hsa_circ_0101145 reverses the epithelial-mesenchymal transition in hepatocellular carcinoma via regulation of the miR-548c-3p/LAMC2 axis

  Relevance score: 6.961606

  Jinglan Jin, Huan Liu, Meishan Jin, Wanyu Li, Hongqin Xu, Feng Wei

  Keywords: hsa_circ_0101145, epithelial-mesenchymal transition, hepatocellular, miR-548c-3p, LAMC2

  Published in Aging on June 18, 2020

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  Hepatocellular carcinoma (HCC) is a primary cause of cancer-related deaths globally. While there have been advancements in HCC treatment and diagnosis, incidence and mortality rates continue to rise. One study found that circular RNAs functioned as competing endogenous RNAs, and constructed a gene-based nomogram to estimate overall survival of HCC patients. Previous studies using high-throughput sequencing suggested that hsa_circ_0101145 is abnormally expressed in HCC, but the underlying mechanism is unknown. We performed RT-qPCR to determine hsa_circ_0101145 and miR-548c-3p expression in HCC tissues. We used fluorescence in situ hybridization (FISH) to detect hsa_circ_0101145 expression and hsa_circ_0101145 subcellular localization in HCC tissues. hsa_circ_0101145 expression in HCC cells was selectively regulated. We determined LAMC2 and EMT mRNA and protein levels by RT-qPCR and western blotting analysis, respectively. We employed flow cytometry, and CCK8, Transwell, and wound healing assays to monitor the cell cycle, cell proliferation, invasion, and migration, respectively. We employed dual-luciferase reporter and RNA pulldown assays to verify the relationship among hsa_circ_0101145, miR-548c-3p, and LAMC2. We examined the effects of hsa_circ_0101145 on HCC cell metastasis and proliferation in vivo using a subcutaneous xenograft model as well as intravenous tail injection of nude mice. The data demonstrated that hsa_circ_0101145 was significantly upregulated in both HCC tissues and cell lines. High hsa_circ_0101145 expression was correlated with aggressive HCC phenotypes. Downregulation of hsa_circ_0101145 suppressed HCC proliferation as well as metastasis by targeting the miR-548c-3p/LAMC2 axis, which was examined using luciferase reporter and RNA pulldown assays. Silencing of hsa_circ_0101145 suppressed the epithelial-mesenchymal transition in HCC. Downregulation of miR-548c-3p or overexpression of LAMC2 restored migration and proliferation abilities of HCC cells following hsa_circ_0101145 silencing. LAMC2 overexpression reversed miR-548c-3p-induced cell migration and growth inhibition in vitro. In summary, the findings illustrated that hsa_circ_0101145 silencing suppressed HCC progression by functioning as an miR-548c-3p sponge to enhance LAMC2 expression. Therefore, hsa_circ_0101145 could be an HCC treatment target.

  

  Expression level and characteristics of the circular RNA hsa_circ_0101145. (A) Genomic loci of the HARS gene and hsa_circ_0101145. (B) Expression and subcellular localization of hsa_circ_0101145 in HCC tissues and adjacent normal tissues was analyzed using in situ hybridization. (C) Expression of hsa_circ_0101145 in HCC tissues (60) and adjacent normal tissues (60) was detected using RT-qPCR. Data are presented as the mean ± SD. ^***P < 0.001 vs. Normal. (D) hsa_circ_0101145 expression in HCC cells lines SMMC7721, Sk-Hep-1, HepG2, and Huh-7 and the human normal liver cell line L02 were analyzed using RT-qPCR. Data are presented as the mean ± SD. ^***P < 0.001 vs. normal cells.

  
  
  

  

  Downregulation of hsa_circ_0101145 suppressed HCC cell proliferation in vivo and in vitro. (A) RT-qPCR detection of hsa_circ_0101145 expression in HepG2 and Huh-7 cells following transfection with siRNA targeting hsa_circ_0101145 (si-circ0101145) or the negative control (NC). Data are presented as the mean ± SD. ^***P < 0.001 vs. NC. (B) Flow cytometry showing the percentages of cells in G1, S, or G2 phase in HepG2 and Huh-7 cells. (C and D) CCK-8 assay showing the proliferation of HepG2 (C) and Huh-7 (D) cells. Data are presented as the mean ± SD. ^**P < 0.01, ^***P < 0.001 vs. NC. (E and F) Colony formation assay showing proliferation of HepG2 and Huh-7 cells. Data are presented as mean ± SD. ^***P < 0.001 vs. NC. (G–J) Western blot analysis of the expression of E-cadherin (epithelial marker), and N-cadherin and vimentin (mesenchymal markers). Data are presented as the mean ± SD. ^***P < 0.001 vs. NC.

  
  
  

  

  Downregulation of hsa_circ_0101145 decreased HCC tumor formation in nude mouse xenografts. (A) Representative images of nude mouse xenografts of HepG2 cells (n = 6). (B) Tumor volumes in mice were measured every 5 days. Data are means ± SD. ^***P < 0.001 vs. NC. (C and D) Western blot analysis of the expression of E-cadherin (epithelial marker), and N-cadherin and vimentin (mesenchymal markers). Data are presented as the mean ± SD. ^***P < 0.001 vs. NC.

  
  
  

  

  Downregulation of hsa_circ_0101145 suppressed tumor metastasis in vivo and in vitro. (A and B) Transwell cell migration assays in HepG2 and Huh-7 cells. Data are means ± SD. ^***P < 0.001 vs. NC. (C and D) Wound-healing assays showing the effect of hsa_circ_0101145 on the closure of scratch wounds. Data are presented as the mean ± SD. ^***P < 0.001 vs. NC. (E) Live imaging shows the effects of hsa_circ_0101145 on the metastasis of HepG2 cells 30 days after intravenous tail injection.

  
  
  

  

  Interactions among hsa_circ_0101145, miR-548c-3p, and LAMC2. (A) RT-qPCR analyses revealed that miR-548c-3p was the only miRNA that was abundantly pulled down by the hsa_circ_0101145 probe in HepG2 cells. Data are presented as means ± SD. ^*P < 0.05, ^**P < 0.01, ^***P < 0.001 vs oligo. (B) RT-qPCR shows the expression of miR-548c-3p in HCC tissues (60) and adjacent normal tissues (60). Data are presented as the mean ± SD. ^***P < 0.001 vs. Normal. (C) Prediction of binding sites of miR-548c-3p in hsa_circ_0101145. The mutant version of hsa_circ_0101145 is presented. (D) Relative luciferase activity determined at 48 h after transfection of 293T cells with miR-548c-3p mimic/NC or hsa_circ_0101145 wild-type/Mut. Data are presented as means ± SD. ^***P < 0.001. (E) Prediction of binding sites of miR-548c-3p in the 3'UTR of LAMC2. The mutant version of 3'UTR-LAMC2 is shown. (F) Relative luciferase activity determined at 48 h after transfection of 293T cells with miR-548c-3p mimic/NC or 3'UTR-LAMC2 wild-type/Mut. Data are presented as means ± SD. ^***P < 0.001.

  
  
  

  

  Downregulation of miR-548c-3p or overexpression of LAMC2 restored the proliferation and migration abilities of both HepG2 and Huh-7 cells following silencing of hsa_circ_0101145. (A–F) RT-qPCR analysis shows the expression of hsa_circ_0101145 (A and B), miR-548c-3p (C and D), and LAMC2 (E and F) in HepG2 and Huh-7 cells following transfection or treatment with NC, si-circ0101145, miR-548c-3p inhibitor, LAMC2 overexpression vector (LAMC2) single or combined. Data are presented as the mean ± SD. ^***P < 0.001 vs. NC. ^###P < 0.001 vs. si-circ0101145. (G–I) Cell proliferation was analyzed by colony formation. Data are presented as the mean ± SD. ^***P < 0.001 vs. NC. ^###P < 0.001 vs. si-circ0101145. (J–L) Cell migration was assessed in HepG2 and Huh-7 cells using Transwell assays. Data are presented as the mean ± SD. ^***P < 0.001 vs. NC. ^###P < 0.001 vs. si-circ0101145. (M and N) Western blot analysis of the expression of E-cadherin, N-cadherin, and vimentin.

  
  
  

  

  LAMC2 overexpression reversed miR-548c-3p-induced cell migration and growth inhibition in vitro. HepG2 and Huh-7 cells were transfected with miR-548c-3p mimics with or without the LAMC2 overexpression vector. (A and B) RT-qPCR assay showing the expression of miR-548c-3p (A and B) and LAMC2 (C and D) in HepG2 and Huh-7 cells. Data are mean ± SD. ^***P < 0.001 versus NC. ^###P < 0.001 versus mimic. (E–G) Colony formation assay showing the proliferation of HepG2 and Huh-7 cells. Data are mean ± SD. ^***P < 0.001. ^###P < 0.001 versus mimic. (H–J) Cell migration were assessed in HepG2 and Huh-7 cells by Transwell assays. Data are mean ± SD. ^***P < 0.001 versus NC. ^###P < 0.001 versus mimic. (K and L) Western blot analysis of the expression of E-cadherin, N-cadherin, and vimentin. Data are mean ± SD. ***P < 0.001 vs. NC. ^###P < 0.001 vs. the mimic.