The knockdown of MTDH expression inhibits human bladder cancer proliferation and invasion through the JAK1/STAT3 signaling pathway in T24 cells

MTDH is overexpressed in many malignant tumors and is closely related to the occurrence and development of tumors. The purpose of this study is to explore the effects of the knockdown of the MTDH gene on the proliferation and metastasis of human bladder cancer in T24 cells. shRNA plasmids targeting MTDH were constructed and transfected into T24 cells. The effects of gene silencing were confirmed by qPCR (Quantitative real-time PCR) and Western blotting. An MTT assay was used to determine the effects of MTDH on the proliferation of the T24 cells. The cell apoptosis rate was determined using Hoechst 33342. We additionally determined the expressions of caspase-3, JAK (Janus Activated Kinase) 1, P-JAK1, STAT (Signal transducers and activators of transcription) 3, P-STAT3, and MTDH using Western blotting, and the secretions of the tumor invasion-related proteins (MMP2 and MMP9) were determined using ELISA. The results showed that MTDH RNAI was constructed and transfected into the T24 cells successfully. Compared to the control groups, the MTDH, P-JAK1, and P-STAT3 proteins were reduced significantly, but the level of caspase-3 was clearly increased in the MTDH RNAI groups. Cell apoptosis was significantly increased in the MTDH RNAI groups. The secretions of MMP2 and MMP9 were decreased, and the cells' ability to proliferate and invade decreased significantly after MTDH RNAI was transfected into the T24 cells. In conclusion, we constructed an shRNA plasmid targeting MTDH, and it was successfully transfected into T24 cells. The knockdown of MTDH expression may inhibit proliferation and invasion via the JAK1/STAT3 pathway in T24 cells. Therefore, MTDH may be a new target for the genetic treatment of human bladder cancer.