Table 3.

Summary for the association between bladder cancer and circadian clock genes

Author	Refs	Study design	Study size	Function	Main result
Litlekalsoy	[144]	Case–control study	27 cases and benign tissues, and 15 normal bladder tissue	Suppressor-Per2, Clock Promoter-Bmal1	BMAL1, CLOCK, and PER1/2/3 in bladder tumor were significantly decreased than neighbouring benign mucosa CRY1 was dramatically upregulated and CRY2 was downregulated in both tumor and neighbouring tissue
Polo	[145]	Bioinformatics tool	no	Suppressor-CSNK1ε	TP53 (HUB node) was tightly correlated to CSNK1ε (circadian node), some other circadian modes was related to other HUB nodes after passing one or two nodes
Jia	[148]	–	Animal and/or cells	Promoter-CRY1	CRY1 was accumulated in quiescent cisplatin-resistant bladder cells while CRY1 knockdown increased PTX-induced senescence Elevated CRY1 in cisplatin-resistant bladder cells induced p53 degradation by promoting FOXO1 binding to its ubiquitin E3 ligase MDM2, which finally preventing PTX-induced senescence
Iyyanki	[149]	–	Animal and/or cells	Suppressor-NPAS2	Overexpressed NPAS2 inhibited trans-well migration in SCABER cell probably via repressing a subset basal maker genes like KRT5, KRT6A, and TFAP2C Higher NPAS2 promoted OS for patients with bladder cancer