title: Aplysin enhances temozolomide sensitivity in glioma cells by increasing miR-181 level.
abstract: OBJECTIVE
  Aplysin, a natural brominate compound from marine organisms, has been demonstrated to exhibit anti-tumor activity, mainly by inducing apoptosis and cell cycle arrest. However, its effect on glioma is still unknown. In this study, we evaluated the effects of aplysin on the malignant properties of glioma cells and its enhancing effect on temozolomide (TMZ) action against drug-resistant glioma cell lines.
  
  
  METHODS
  We employed several human glioma cell lines and primary glioma cells to address this issue with multidisciplinary approaches.
  
  
  RESULTS
  The combined application of aplysin and TMZ significantly sensitizes glioma cells to TMZ action, compared with TMZ alone. miRNA profile analysis revealed that the abundance of miR-181, an important glioma tumor suppressors believed to enhance TMZ effect, was greatly elevated in aplysin-treated glioma cell lines. The aplysin-induced TMZ sensitivity is dependent on MEK1 in glioma cells. Overexpression of MEK1 was able to abolish the effect of aplysin on glioma cells.
  
  
  CONCLUSIONS
  We found that aplysin can enhance the effect of TMZ on glioma cells by increasing miR-181 expression.
authors.affiliation: Department of Neurosurgery, The Affiliated Hospital of Qingdao University, Qingdao, 266003, China.
authors.forename: Anjing
authors.initials: A
authors.lastname: Gong
authors.forename: Na
authors.initials: N
authors.lastname: Ge
authors.forename: Weicheng
authors.initials: W
authors.lastname: Yao
authors.forename: Luxiang
authors.initials: L
authors.lastname: Lu
authors.forename: Hui
authors.initials: H
authors.lastname: Liang
mesh_terms: D000818:Animals; D018906:Antineoplastic Agents, Alkylating / Q000494:pharmacology*; D000971:Antineoplastic Combined Chemotherapy Protocols / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects; D001932:Brain Neoplasms / Q000188:drug therapy* / Q000235:genetics / Q000473:pathology; D045744:Cell Line, Tumor; D003606:Dacarbazine / Q000031:analogs & derivatives* / Q000494:pharmacology; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects; D005910:Glioma / Q000188:drug therapy* / Q000235:genetics / Q000473:pathology; D006801:Humans; D006842:Hydrocarbons, Brominated / Q000494:pharmacology*; D048369:MAP Kinase Kinase 1 / Q000235:genetics / Q000378:metabolism; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D035683:MicroRNAs / Q000235:genetics*; D012717:Sesquiterpenes / Q000494:pharmacology*; D000077204:Temozolomide; D023041:Xenograft Model Antitumor Assays
chemical_list: D018906:Antineoplastic Agents, Alkylating; D006842:Hydrocarbons, Brominated; C540193:MIrn181 microRNA, human; D035683:MicroRNAs; D012717:Sesquiterpenes; D003606:Dacarbazine; D048369:MAP Kinase Kinase 1; C482125:MAP2K1 protein, human; C000592510:aplysin; D000077204:Temozolomide