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Significance: Speckle variation induced by intracellular motion (IM) in the urothelium was observed in optical coherence tomography (OCT) images. IM can be used as a dynamic contrast to segment the urothelium by comparing two sequential OCT images. This method opens the possibility of specifically tracking the distribution of urothelial cancerous cells for identifying the microinvasion of bladder tumors., Approach: OCT images were acquired ex vivo with fresh porcine bladder tissue. IM was analyzed by tracking speckle variation using autocorrelation function, then quantified with constrained regularization method for inverting data (CONTIN method) to identify the decorrelation time (DT) of the speckle variations. Variance analysis was also conducted to show IM amplitude and distribution in the urothelium. The segmentation of the urothelium was demonstrated with OCT images with a visible urothelial layer and OCT images with an invisible urothelial layer., Results: Significant speckle variation induced by IM was observed in the urothelium. However, the distribution of the IM is heterogeneous. The DTs are mostly concentrated between 1 and 30 ms. With the IM as a dynamic contrast, the urothelium can be accurately and exclusively segmented, even the urothelial layer is invisible in normal OCT images., Conclusions: IM can be used as a dynamic contrast to exclusively track urothelial cell distribution. This contrast may provide a new mechanism for OCT to image the invasion depth and pattern of urothelial cancerous cells for accurately substaging of bladder cancer.

Bladder cancer (BC) is the ninth most frequent malignancy and the thirteenth leading cause of cancer-related death worldwide. CDKN1A-interacting zinc finger protein 1 (CIZ1) is involved in the development of various cancers, while its role in BC remains unclear. In this study, we found that CIZ1 was up-regulated in BC tissues and cells. Knockdown of CIZ1 suppressed the proliferation and growth of T24 and 5637 cells. Apoptosis and caspase 3/7 activity were enhanced after CIZ1 silencing in both cells. At the molecular level, PCNA, Ki67, HIF-1α, survivin, CCND1 and CCNB1 were down-regulated, and caspase-3, p53, p21, caspase-9 were up-regulated by CIZ1 knockdown. This suggested that silencing of CIZ1 suppressed BC cell proliferation through inducing apoptosis and reducing cell cycle progression. Our study suggests that targeting CIZ1 maybe a potential therapeutic strategy for BC., (Copyright © 2019. Published by Elsevier B.V.)