Author: Tan, Zhaoli; Gao, Lihua; Wang, Yan; Yin, Huihui; Xi, Yongyi; Wu, Xiaojie; Shao, Yong; Qiu, Weiyi; Du, Peng; Shen, Wenlong; Fu, Ling; Jia, Ru; Zhao, Chuanhua; Zhang, Yun; Zhao, Zhihu; Sun, Zhiwei; Chen, Hongxing; Hu, Xianwen; Xu, Jianming; Wang, Youliang
Title: PRSS contributes to cetuximab resistance in colorectal cancer Document date: 2020_1_1
ID: tymoeyoo_29
Snippet: Our results described above and those of previous studies by others show that SPINK1 is an efficient trypsin inhibitor (32) that partially inhibits the proteolytic cleavage of mAbs by PRSS1. We hypothesized that combined treatment with SPINK1, which we purified, and cetuximab or bevacizumab may lead to a supra-additive reduction in colon cancer cell growth. Accordingly, we tested the effect of SPINK1 (10 ng/ml) and cetuximab (1 or 5 ïg/ml) on H.....
Document: Our results described above and those of previous studies by others show that SPINK1 is an efficient trypsin inhibitor (32) that partially inhibits the proteolytic cleavage of mAbs by PRSS1. We hypothesized that combined treatment with SPINK1, which we purified, and cetuximab or bevacizumab may lead to a supra-additive reduction in colon cancer cell growth. Accordingly, we tested the effect of SPINK1 (10 ng/ml) and cetuximab (1 or 5 ïg/ml) on HT-29 cell proliferation. As expected, SPINK1 and cetuximab (5 ïg/ml) significantly decreased HT-29 cell viability (Fig. 5A) . Consistent with previous reports (32), purified SPINK1 also significantly increased HT-29 cell proliferation (Fig. 5A) .
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