title: TP53INP2-related basal autophagy is involved in the growth and malignant progression in human liposarcoma cells.
abstract: BACKGROUND
  Understanding the function of autophagy may allow us to develop a promising therapeutic strategy to enhance the effects of chemotherapy and improve clinical outcomes in the treatment of cancers. Here, we studied the contribution of basal autophagy in human liposarcoma.
  
  
  METHODS
  The levels of basal autophagy were analyzed by measuring autophagy-related protein expression and autophagosome formation. TP53INP2 expression was determined by real-time PCR, western blot and tissue microarray. Genetic inhibition or overexpression of TP53INP2 was performed to examine its effects on autophagic activity and cell growth.
  
  
  RESULTS
  Compared with human liposarcoma cell line SW872, low level of basal autophagy were present in SW872-S cells with high malignancy. Moreover, a decrease of TP53INP2 expression was found accompanying liposarcoma malignant progression in cell lines and primary tissues. TP53INP2 expression was required for autophagic activity in liposarcoma cells. Autophagy inhibition with chloroquine suppressed the growth of liposarcoma cells. TP53INP2-related basal autophagy rendered liposarcoma cells to be more resistant to bortezomib-induced inhibition of cell growth.
  
  
  CONCLUSIONS
  The results reveal the association of TP53INP2-related basal autophagy with cell growth and malignant progression of human liposarcoma, which helps re-evaluate targeting autophagy for cancer therapy, and suggest that TP53INP2 expression might be used as a prognostic marker to predict human liposarcoma malignancies.
authors.affiliation: State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing 210093, China.
authors.forename: Yamei
authors.initials: Y
authors.lastname: Hu
authors.affiliation: State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing 210093, China.
authors.forename: Xin
authors.initials: X
authors.lastname: Li
authors.affiliation: State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing 210093, China.
authors.forename: Wenwen
authors.initials: W
authors.lastname: Xue
authors.affiliation: State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing 210093, China.
authors.forename: Juan
authors.initials: J
authors.lastname: Pang
authors.affiliation: State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing 210093, China.
authors.forename: Yiwei
authors.initials: Y
authors.lastname: Meng
authors.affiliation: State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing 210093, China. Electronic address: shenyan@nju.edu.cn.
authors.forename: Yan
authors.initials: Y
authors.lastname: Shen
authors.affiliation: State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing 210093, China. Electronic address: molpharm@163.com.
authors.forename: Qiang
authors.initials: Q
authors.lastname: Xu
mesh_terms: D000818:Animals; D001343:Autophagy / Q000187:drug effects; D000069286:Bortezomib / Q000494:pharmacology; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D018450:Disease Progression; D019008:Drug Resistance, Neoplasm / Q000187:drug effects; D006801:Humans; D008080:Liposarcoma / Q000378:metabolism* / Q000473:pathology*; D008819:Mice, Nude; D009687:Nuclear Proteins / Q000378:metabolism*; D034741:RNA, Small Interfering / Q000378:metabolism; D014162:Transfection
chemical_list: D009687:Nuclear Proteins; D034741:RNA, Small Interfering; C501283:TP53INP2 protein, human; D000069286:Bortezomib
keywords: Autophagy; Human liposarcoma; Malignant progression; SW872 cells; TP53INP2