ALPK2 acts as tumor promotor in development of bladder cancer through targeting DEPDC1A

• Published in: Cell death & disease Vol. 12; no. 7; p. 661
• Main Authors: Wang, Yuchen, Wu, Jie, Luo, Wenjie, Zhang, Hailiang, Shi, Guohai, Shen, Yijun, Zhu, Yao, Ma, Chunguang, Dai, Bo, Ye, Dingwei, Zhu, Yiping
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 01.07.2021; Springer Nature B.V; Nature Publishing Group
• Subjects: 13/1; 13/109; 13/2; 13/31; 13/51; 38/5; 38/77; 38/90; 38/91; 631/67/589/1336; 631/67/70; 64/60; Animals; Antibodies; Apoptosis; Biochemistry; Biomedical and Life Sciences; Bladder cancer; Cancer; Cell Biology; Cell Culture; Cell Line, Tumor; Cell migration; Cell Movement; Cell Proliferation; Databases, Genetic; Gene Expression Regulation, Neoplastic; GTPase-Activating Proteins - genetics; GTPase-Activating Proteins - metabolism; Humans; Immunology; Life Sciences; Mice; Mice, Inbred BALB C; Mice, Nude; Neoplasm Invasiveness; Neoplasm Proteins - genetics; Neoplasm Proteins - metabolism; Protein Kinases - genetics; Protein Kinases - metabolism; Signal Transduction; Tumors; Urinary Bladder Neoplasms - enzymology; Urinary Bladder Neoplasms - genetics; Urinary Bladder Neoplasms - pathology
• ISSN: 2041-4889; 2041-4889
• DOI: 10.1038/s41419-021-03947-7

Bladder cancer is one of the most common malignant tumors in the urinary system. The development and improvement of treatment efficiency require the deepening of the understanding of its molecular mechanism. This study investigated the role of ALPK2, which is rarely studied in malignant tumors, in the development of bladder cancer. Our results showed the upregulation of ALPK2 in bladder cancer, and data mining of TCGA database showed the association between ALPK2 and pathological parameters of patients with bladder cancer. In vitro and in vivo experiments demonstrated that knockdown of ALPK2 could inhibit bladder cancer development through regulating cell proliferation, cell apoptosis, and cell migration. Additionally, DEPDC1A is identified as a potential downstream of ALPK2 with direct interaction, whose overexpression/downregulation can inhibit/promote the malignant behavioral of bladder cancer cells. Moreover, the overexpression of DEPDC1A can rescue the inhibitory effects of ALPK2 knockdown on bladder cancer. In conclusion, ALPK2 exerts a cancer-promoting role in the development of bladder cancer by regulating DEPDC1A, which may become a promising target to improve the treatment strategy of bladder cancer.