title: Silencing CAPN2 Expression Inhibited Castration-Resistant Prostate Cancer Cells Proliferation and Invasion via AKT/mTOR Signal Pathway.
abstract: The mRNA expression of CAPN2 was upregulated in CRPC cells (DU145 and PC3) than that in non-CRPC cells. Silencing CAPN2 expression could inhibit DU145 and PC3 cells proliferation by cell cycle arrest at G1 phase. Knockdown of CPAN2 level suppressed the migration and invasion capacity of CRPC cells by reducing matrix metalloproteinase-2 (MMP-2) and MMP-9 activation, as well as repressing the phosphorylation protein expression of AKT and mTOR. In addition, we found that the expression of CAPN2 was elevated in Pca tissues than that in normal control tissues. Therefore, we showed the important roles of CAPN2 in the development and progression in CRPC cells, suggesting a new therapeutic intervention for treating castration-resistant prostate cancer patients.
authors.affiliation: State Key Laboratory of Reproductive Medicine and Department of Urology, The First Affiliated Hospital, Nanjing Medical University, Nanjing 210029, China.
authors.forename: Pu
authors.initials: P
authors.lastname: Li
authors.affiliation: State Key Laboratory of Reproductive Medicine and Department of Urology, The First Affiliated Hospital, Nanjing Medical University, Nanjing 210029, China.
authors.forename: Chenkui
authors.initials: C
authors.lastname: Miao
authors.affiliation: State Key Laboratory of Reproductive Medicine and Department of Urology, The First Affiliated Hospital, Nanjing Medical University, Nanjing 210029, China.
authors.forename: Chao
authors.initials: C
authors.lastname: Liang
authors.affiliation: State Key Laboratory of Reproductive Medicine and Department of Urology, The First Affiliated Hospital, Nanjing Medical University, Nanjing 210029, China.
authors.forename: Pengfei
authors.initials: P
authors.lastname: Shao
authors.affiliation: State Key Laboratory of Reproductive Medicine and Department of Urology, The First Affiliated Hospital, Nanjing Medical University, Nanjing 210029, China.
authors.forename: Zengjun
authors.identifier: 0000-0001-7224-3341
authors.initials: Z
authors.lastname: Wang
authors.affiliation: State Key Laboratory of Reproductive Medicine and Department of Urology, The First Affiliated Hospital, Nanjing Medical University, Nanjing 210029, China.
authors.forename: Jie
authors.identifier: 0000-0003-0260-1611
authors.initials: J
authors.lastname: Li
mesh_terms: D000368:Aged; D002154:Calpain / Q000235:genetics* / Q000378:metabolism; D002465:Cell Movement / Q000235:genetics; D049109:Cell Proliferation / Q000235:genetics; D015972:Gene Expression Regulation, Neoplastic; D055785:Gene Knockdown Techniques; D020868:Gene Silencing; D006801:Humans; D008297:Male; D020778:Matrix Metalloproteinase 2 / Q000378:metabolism; D020780:Matrix Metalloproteinase 9 / Q000378:metabolism; D008875:Middle Aged; D009361:Neoplasm Invasiveness; D064129:Prostatic Neoplasms, Castration-Resistant / Q000201:enzymology / Q000235:genetics* / Q000473:pathology*; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D060888:Real-Time Polymerase Chain Reaction; D015398:Signal Transduction / Q000235:genetics; D058570:TOR Serine-Threonine Kinases / Q000378:metabolism*; D014945:Wound Healing / Q000235:genetics
chemical_list: D012333:RNA, Messenger; D051057:Proto-Oncogene Proteins c-akt; D058570:TOR Serine-Threonine Kinases; D002154:Calpain; C569870:CAPN2 protein, human; D020778:Matrix Metalloproteinase 2; D020780:Matrix Metalloproteinase 9