z-logo
open-access-imgOpen Access
KLK4 Silencing Inhibits the Growth of Chromophobe Renal Cell Carcinoma through ERK/AKT Signaling Pathway
Author(s) -
Fan Bo,
Niu Yunfeng,
Zhang Aili,
Wei Shufei,
Ma Yongliang,
Su Jianzhi,
Ren Zongtao
Publication year - 2022
Publication title -
kidney and blood pressure research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.806
H-Index - 51
eISSN - 1423-0143
pISSN - 1420-4096
DOI - 10.1159/000527412
Subject(s) - research article
Renal cell carcinoma (RCC) generally has a poor prognosis because of late diagnosis and metastasis. Despite its abundance in RCC cells, the functions of kallikrein-related peptidase 4 (KLK4) in RCC cells remain unknown. The results of this investigation were examined to discover if KLK4 gene silencing influences the development of RCC cells. Methods: The mRNA levels of KLK4 and the relationship between KLK4 and tumor stage in patients with RCC were analyzed from the GEPIA database. Real-time PCR and Western blotting were used to measure the mRNA and protein levels of KLK4. Cell Counting Kit 8 (CCK-8), colony formation, wound healing, and Transwell assays were used to examine the proliferation, invasion, and migration of RCC cells after KLK4 suppression. Finally, xenograft experiments in a mouse model helped understand the in vivo effects of KLK4 knockdown. Results: Our research found that KLK4 expression was upregulated in the kidney chromophobe (KICH) specimens and cell lines. Moreover, inhibiting KLK4 growth led to a slowdown in RCC cell proliferation and colony formation. Additionally, KLK4 knockdown inhibited migration, invasion, and epithelial-mesenchymal transition (EMT) of RCC cells. AKT and ERK phosphorylation were enhanced with KLK4 silencing. In the nude mouse xenograft cancer model, KLK4 silencing also prevented the expression of Ki-67, CD105, and the growth of tumors. Conclusion: KLK4 accelerated KICH progression via the ERK/AKT signaling pathway, providing a novel regulatory mechanism for KICH pathogenesis.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.
Having issues? You can contact us here