title: Silencing of Cathepsin B suppresses the proliferation and invasion of endometrial cancer.
abstract: The molecular mechanism involved in the metastasis of endometrial cancer (EC) remains unclear. The lysosomal cysteine protease Cathepsin B has been implicated in the progression of various human tumors. In the present study, we assessed the expression of Cathepsin B and its functions in EC. Immunohistochemistry was used to examine Cathepsin B expression in 76 paraffin-embedded endometrial tumor tissues. Lentiviral packing short hairpin RNA (shRNA) was transfected into HEC-1A cells to build a stable Cathepsin B knockdown cell line. The cellular levels of Cathepsin B mRNA and protein were detected by real-time PCR and western immunoblotting. The functions of Cathepsin B in EC cells were measured by MTT, migration and invasion assays. In additon, tumorigenicity assays were established in nude mice to study tumor growth in vivo. The results of our study showed that Cathepsin B was overexpressed in EC tissues compared with normal endometrium and endometrial atypical hyperplasia. Depletion of Cathepsin B in vitro inhibited cell proliferation, migration and invasion. Tumor formation assays confirmed that suppression of Cathepsin B inhibited the proliferation potential of HEC-1A cells in vivo, demonstrated by lower proliferation rates. These results suggest that Cathepsin B may act as an oncogene in EC, with the potential to provide a new therapeutic target for treating endometrial malignancy.
authors.affiliation: Department of Obstetrics and Gynecology, International Peace Maternity and Child Health Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200030, PR China.
authors.forename: Wei
authors.initials: W
authors.lastname: Bao
authors.forename: Qiong
authors.initials: Q
authors.lastname: Fan
authors.forename: Xin
authors.initials: X
authors.lastname: Luo
authors.forename: Wei-Wei
authors.initials: WW
authors.lastname: Cheng
authors.forename: Yu-Dong
authors.initials: YD
authors.lastname: Wang
authors.forename: Zhu-Nan
authors.initials: ZN
authors.lastname: Li
authors.forename: Xin-Liang
authors.initials: XL
authors.lastname: Chen
authors.forename: Dan
authors.initials: D
authors.lastname: Wu
mesh_terms: D000818:Animals; D015197:Carcinogenicity Tests / Q000379:methods; D002401:Cathepsin B / Q000096:biosynthesis / Q000172:deficiency* / Q000235:genetics* / Q000378:metabolism; D045744:Cell Line, Tumor; D002465:Cell Movement; D049109:Cell Proliferation; D004714:Endometrial Hyperplasia / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D016889:Endometrial Neoplasms / Q000235:genetics* / Q000378:metabolism / Q000473:pathology*; D004717:Endometrium / Q000378:metabolism / Q000473:pathology; D005260:Female; D055785:Gene Knockdown Techniques; D006801:Humans; D051379:Mice; D008807:Mice, Inbred BALB C; D008819:Mice, Nude; D008875:Middle Aged; D009361:Neoplasm Invasiveness; D012333:RNA, Messenger / Q000235:genetics
chemical_list: D012333:RNA, Messenger; C533912:CTSB protein, human; D002401:Cathepsin B