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• Research Paper Volume 11, Issue 22 pp 10144-10153

  Long noncoding RNA LINC00899 suppresses breast cancer progression by inhibiting miR-425

  Relevance score: 7.682593

  Wenying Zhou, Jiao Gong, Yaqiong Chen, Jiahao Chen, Qi Zhuang, Jing Cao, Zhixiong Mei, Bo Hu

  Keywords: breast cancer, LINC00899, proliferation, miR-425, DICER

  Published in Aging on November 18, 2019

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  Long non-coding RNAs (lncRNAs) have emerged as important regulators in cancer, including breast cancer. The precise expression pattern of long noncoding RNA 00899 (LINC00899) in breast cancer and its mechanisms of action have not been reported. Here, we found that LINC00899 is downregulated in breast cancer tissues and cell lines. Kaplan-Meier analysis showed that elevated LINC00899 expression is closely associated with better relapse-free survival (RFS) in breast cancer, including the basal, luminal A or luminal B breast cancer subtypes. Gene Ontology terms and Kyoto Encyclopedia of Genes and Genomes pathway analysis suggested that LINC00899 is closely related to several cancer associated processes, including tight junction- and metabolism-associated pathways. Functional assays indicated that LINC00899 overexpression suppresses proliferation, migration and invasion of breast cancer cells in vitro. Moreover, LINC00899 was found to competitively bind miR-425, thereby functioning as a tumor suppressor by enhancing DICER1. Overexpression of miR-425 attenuated the LINC00899-induced inhibition of breast cancer cell proliferation and invasion. These findings highlight the important role of the LINC00899-miR-425-DICER1 axis in breast cancer cell proliferation and invasion, and could potentially lead to new lncRNA-based diagnostics or therapeutics for breast cancer.

  

  LINC00899 is downregulated in human breast cancer tissues and cell lines. (A) Comparison of the relative LINC00899 expression levels between 26 pairs of breast cancer (BC) tissues and adjacent normal tissues. (B) Comparison of the relative LINC00899 expression levels between the normal human mammary epithelial cells (MCF-10A) and 5 BC cell lines. Data presented as means ± SD, *p< 0.05, **p< 0.01.

  
  
  

  

  High LINC00899 levels correlate with a better prognosis in breast cancer patients. (A–C) Kaplan–Meier survival curve analysis performed using KM plotter. Breast cancer patients were divided into two equal groups based on median expression value of LINC00899. The hazard ratio (HR) and log-rank p-value comparing the two groups are shown. Low and high risks are indicated in black and red, respectively.

  
  
  

  

  KEGG and GO analysis of the genes relevant to LINC00899 in breast cancer. (A) KEGG pathway enrichment for LINC00899. (B–D) Molecular functions, cell components and biological processes. These results were retrieved from the circlncRNAnet.

  
  
  

  

  Overexpression of LINC00899 inhibits BC cell proliferation, colony formation, migration and invasion. (A) MDA-MB-231 and SKBR3 cells were transfected with LINC00899-carrying lentivirus (Lv-LINC00899) or control lentivirus (Lv-control) followed by qRT-PCR analysis of the relative LINC00899 expression levels. (B–E) Cells transfected with Lv-control, Lv-LINC00899 or Lv-LINC00899 plus miR-425 mimic. CCK8 (B) and colony formation (C) assays were used to assess proliferation of MDA-MB-231 and SKBR3 cells. Wound healing assays were performed to assess migration of MDA-MB-231 (D) and SKBR3 (E) cells. Transwell invasion assays were performed to assess invasion by MDA-MB-231and SKBR3cells (F). Data presented as means ± SD.**p< 0.01.

  
  
  

  

  LINC00899 directly binds to miR-425 in breast cancer. (A–B) Bioinformatic analysis of the potential miR-425 binding sites within wild-type LINC00899-1 (LINC00899 WT-1) or LINC00899-2 (LINC00899 WT-2). (C–D) Luciferase reporter vectors containing WT-1 (left) or WT-2 (right) as well as corresponding mutant (Mut, Mut-1 or Mut-2) miR-425 binding sequences were cotransfected into BC cell lines (MDA-MB-231 and SKBR3) together with miR-425 mimic or NC mimic. Dual-luciferase reporter assays were performed to assess the luciferase activity in MDA-MB-231 and SKBR3 cells expressing luciferase fused to WT-LINC00899 or Mut-LINC00899. (E) Spearman’s analysis of the correlation between LINC00899 and miR-425 levels in BC tissues. Data are presented as means ± SD, *p< 0.01. (F) Western blot analysis of DICER1, CDH1 and VIM expression in MDA-MB-231 and SKBR3 cells transfected with Lv-control, Lv-LINC00899 or Lv-LINC00899 plus miR-425 mimic. (G–H) qRT-PCR analysis of miR-425 and DICER1 expression in MDA-MB-231 and SKBR3 cells transfected with Lv-control or Lv-LINC00899. (I) Expression of LINC00899 in cells transfected with miR-control or miR-425 mimic. Data presented as means ± SD, *p< 0.01.