Silencing of Cathepsin B suppresses the proliferation and invasion of endometrial cancer

Abstract

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.

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“…ULK3 serves as a regulator in sonic hedgehog (SHH) signaling and autophagy in humans ( Young et al, 2009 ; Maloverjan et al, 2010 ). CTSB was found to participate in autophagy and immune resistance, which could be a potentially biomarker for various cancers ( Bao et al, 2013 ; Mirkovic et al, 2015 ; Bian et al, 2016 ).…”

Dietary Compound Isoliquiritigenin, an Antioxidant from Licorice, Suppresses Triple-Negative Breast Tumor Growth via Apoptotic Death Program Activation in Cell and Xenograft Animal Models

“…Cathepsin B is a lysosomal protease and is related to autophagy progression and p62 degradation [45]. Cancer studies have shown that cathepsin B is related to cancer cell proliferation [46], and its ability to break down the cell base membrane can increase cancer cell invasion. Our results show that ISL can decrease cathepsin B protein expression to suppress p62 accumulation, increasing autophagy-mediated apoptosis and decreasing cancer cell proliferation-related Ki67 expression.…”

Cathepsin K modulates invasion, migration and adhesion of oral squamous cell carcinomas in vitro

“…Cathepsins B and L are known to have opposite effects on cellular proliferation. For example, knockdown of cathepsin B with shRNA inhibits cell proliferation, migration and invasion in endometrial cancer cells (Bao et al , ). Similarly, downregulation of cathepsin L with RNA interference impairs cell proliferation.…”