Knockdown of KLK12 inhibits viability and induces  apoptosis in human colorectal cancer HT-29 cell line.

Knockdown of KLK12 inhibits viability and induces apoptosis in human colorectal cancer HT-29 cell line. Int J Mol Med. 2019 Aug 30;: Authors: Li Q, Zhou X, Fang Z, Zhou H Abstract Kallikrein‑related peptidase 12 (KLK12) is overexpressed in cancer tissues including gastric, breast and prostate cancer. However, the role of KLK12 in colorectal cancer is not fully understood. In the present study, the level of KLK12 was determined by performing reverse transcription‑polymerase chain reaction (RT‑qPCR) in colorectal cancer tissues and cell lines. Lipofectamine® 2000 was used to transfect HT‑29 cells to overexpress and knockdown KLK12. Cell viability, migration, invasion and apoptosis were detected by MTT, wound healing, Transwell and flow cytometry assays, respectively. The mRNA and protein expression levels of EMT‑associated proteins, apoptosis‑associated proteins, phosphorylated adenosine monophosphate‑activated protein kinase (p‑AMPK) and phosphorylated mammalian target of rapamycin (p‑mTOR) were determined by RT‑qPCR and western blot analysis. It was identified that the KLK12 mRNA levels were increased significantly in colorectal cancer tissues and cell lines. KLK12 small interfering RNA inhibited cell viability, migration and invasion. Furthermore, epithelial‑mesenchymal transition (EMT)‑associated proteins were altered by siKLK12. Cell apoptosis was induced by KLK12 downregulation, which was demonstrated by...
Source: International Journal of Molecular Medicine - Category: Molecular Biology Authors: Tags: Int J Mol Med Source Type: research