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Optical multiplexing attracts considerable attention in the field of information encryption, optical probe, and time‐resolved bioimaging. However, the optical multiplexing based on rare‐earth nanoparticles suffers from heavy metal elements and relatively short lifetimes; sophisticated facilities are thus needed. Herein, time division duplexing based on eco‐friendly carbon nanodots (CNDs) with manipulative luminescence lifetimes is demonstrated. In a single green color emission channel, the luminescence lifetimes of the CNDs can be manipulated from nanosecond level to second level by introducing water, while the lifetime of the CNDs confined by a silica shell stays. Time division duplexing based on the CNDs and CNDs@silica with distinct lifetimes is realized and spatio‐temporal overlapping information is thus resolved. High‐level information encryption using the time division duplexing technology is realized. This work may promise the potential applications of CNDs in multi‐lifetime channels biological imaging, high‐density information storage, and anti‐counterfeiting. [ABSTRACT FROM AUTHOR]

(C) The invasion abilities of BECN1 knockdown in UMUC3 cells were evaluated in comparison to their vector transfectants using a BD BioCoatTM MatrigelTM Invasion Chamber applied with the matrigel. ATG7 Promotes Bladder Cancer Invasion via Autophagy-Mediated Increased ARHGDIB mRNA Stability A) The invasion abilities of the indicated cells were evaluated. gl GLO:I6Z7/17nov21:advs202104365-fig-0003.jpg PHOTO (COLOR): S1 (A) The potential microRNAs binding sites in ATG7 mRNA 3'-UTR were analyzed using the TargetScan, PicTar, and miRanda databases. [Extracted from the article]

Since invasive bladder cancer (BC) can progress to life threatening metastases, understanding the molecular mechanisms underlying BC invasion is crucial for potentially decreasing the mortality of this disease. Herein, it is discovered that autophagy‐related gene 7 (ATG7) is remarkably overexpressed in human invasive BC tissues. The knockdown of ATG7 in human BC cells dramatically inhibits cancer cell invasion, revealing that ATG7 is a key player in regulating BC invasion. Mechanistic studies indicate that MIR190A is responsible for ATG7 mRNA stability and protein overexpression by directly binding to ATG7 mRNA 3′‐UTR. Furthermore, ATG7‐mediated autophagy promotes HNRNPD (ARE/poly(U)‐binding/degradation factor 1) protein degradation, and in turn reduces HNRNPD interaction with ARHGDIB mRNA, resulting in the elevation of ARHGDIB mRNA stability, and subsequently leading to BC cell invasion. The identification of the MIR190A/ATG7 autophagic mechanism regulation of HNRNPD/ARHGDIB expression provides an important insight into understanding the nature of BC invasion and suggests that autophagy may represent a potential therapeutic strategy for the treatment of human BC patients. [ABSTRACT FROM AUTHOR]