Clusteroluminogens (CLgens), nonconjugated structures with visible luminescence at the clustering state, have recently received remarkable attention due to their great theoretical significance and practical values. In carbonyl‐based aliphatic polymers, (n, π*) transition of carbonyl groups and the through‐space interactions have been demonstrated to play an important role in their clusteroluminescence (CL) properties, but it is still a big challenge to manipulate their CL at the molecular level. In this work, six nonconjugated carbonyl‐based polymers with different heteroatoms and steric hindrances were synthesized, and their photophysical properties were systematically studied. These polymers all showed CL but with different emission efficiency and wavelength. Experimental and theoretical studies indicated that the CL properties could be manipulated by changing the electronic structures of carbonyl groups and the rigidity of polymer chains. This work not only gains further insights into the CL mechanism but also provides reliable strategies to design and manipulate non‐conjugated luminescent materials.

These authors contributed equally to this workPurpose: Previous studies have identified the important roles of a long noncoding RNA called FGD5 antisense RNA 1 (FGD5-AS1) in several types of human cancer. Nonetheless, to our knowledge, the expression and functions of FGD5-AS1 in esophageal squamous cell carcinoma (ESCC) have not been clarified. In this study, we aimed to determine the expression status of long noncoding RNA FGD5-AS1 in ESCC, determine its participation in ESCC progression, and uncover the underlying mechanisms. Methods: ESCC tissue samples and paired normal adjacent tissues were collected to quantify FGD5-AS1 expression by reverse-transcription quantitative PCR. The effects of FGD5-AS1 on ESCC cell proliferation, apoptosis, migration, and invasion in vitro as well as tumor growth in vivo were studied using a Cell Counting Kit-8 assay, flow cytometry, Transwell migration and invasion assays, and an in vivo tumor xenograft experiment. Results: FGD5-AS1 was found to be aberrantly upregulated in both ESCC tumors and cell lines compared to the control groups. Increased FGD5-AS1 expression manifested a close association with tumor size, TNM stage, and lymph node metastasis in patients with ESCC. Overall survival of patients with ESCC was shorter in the FGD5-AS1 high-expression group than in the FGD5-AS1 low-expression group. An FGD5-AS1 knockdown markedly attenuated ESCC cell proliferation, migration, and invasion and promoted apoptosis in vitro as well as slowed tumor growth in vivo. Mechanism investigation revealed that FGD5-AS1 can increase SP1 expression by sponging microRNA-383 (miR-383), thus functioning as a competing endogenous RNA. An miR-383 knockdown and recovery of SP1 expression attenuated the inhibition of the malignant characteristics of ESCC cells by the FGD5-AS1 knockdown. Conclusion: Thus, FGD5-AS1 enhances the aggressive phenotype of ESCC cells in vitro and in vivo via the miR-383-SP1 axis, which may represent a novel target for ESCC therapy.

Nonconjugated and nonaromatic heteroatoms-based structures are discovered with visible emission at clustering state, namely clusteroluminogens (CLgens).Such kind of luminescence is termed clusteroluminescence (CL) which could not be explained by the traditional molecular photophysical theories constructed upon through-bond conjugation, so investigation on CL has great theoretical significance. In this perspective, we summarize a general feature for C═O bond-based CLgens that a magic blue emission around 440 nm widely exists in different systems such as natural protein, polyamide, polyester, and polyketone. Comprehensive analysis of the reported works suggests that the (n, π*) transition of carbonyl group most likely generates the 440 nm CL. This perspective aims to draw researchers' attention to the common features and general photophysical theories of CL, and shine new light on aggregate photophysics.

Plasma cell-free DNA (cfDNA) are small molecules generated through a non-random fragmentation procedure. Despite commendable translational values in cancer liquid biopsy, however, the biology of cfDNA, especially the principles of cfDNA fragmentation, remains largely elusive. Through orientation-aware analyses of cfDNA fragmentation patterns against the nucleosome structure and integration with multidimensional functional genomics data, here we report a DNA methylation – nuclease preference – cutting end – size distribution axis, demonstrating the role of DNA methylation as a functional molecular regulator of cfDNA fragmentation. Hence, low-level DNA methylation could increase nucleosome accessibility and alter the cutting activities of nucleases during DNA fragmentation, which further leads to variation in cutting sites and size distribution of cfDNA. We further develop a cfDNA ending preference-based metric for cancer diagnosis, whose performance has been validated by multiple pan-cancer datasets. Our work sheds light on the molecular basis of cfDNA fragmentation towards broader applications in cancer liquid biopsy.