Summary As one of the worst invasive weeds in the world, Mikania micrantha H. B. K. spread to southern China after 1910 but without any natural enemies. Since the 1980s it has started to spread and invade widely. The weed has caused significant damage to many ecosystems in Guangdong province in recent years. This paper reviews the research in China on this weed, including its description, history of introduction together with information from morphological and physiological studies. The distribution of this invasive plant in China has been mapped and is presented together with damage being caused and analyses of soil types infested. The measures taken by the Chinese government for prevention and elimination are also discussed. Chinese scientists are now looking for effective biocontrol options to deal with this deleterious plant. Several native insects, mites and fungi have been reported to be able to control the reproduction of this weed in China, but no natural control has been achieved. Cuscuta sp., a native autoecious vine has recently been shown to suppress the growth of M. micrantha. Three major causes for the massive spread of this weed in southern China are presented together with recommendations for future control activities.

Background: Circular RNAs (circRNAs) are a novel class of endogenous noncoding RNAs formed by a covalently closed loop, and increasing evidence has revealed that circRNAs play crucial functions in regulating gene expression. CircSLC8A1 is a circRNA generated from the SLC8A1 gene. Currently, the role and underlying molecular mechanisms of circSLC8A1 in bladder cancer remain unknown. Methods: The differentially expressed circRNAs were identified from RNA-sequencing data, and circSLC8A1 was determined as a new candidate circRNA. qRT-PCR was used to detect the expression of circRNAs, miRNAs and mRNAs in human tissues and cells. RNA pull-down assay and luciferase reporter assay were used to investigate the interactions between the specific circRNA, miRNA and mRNA. The effects of circSLC8A1 on bladder cancer cells were explored by transfecting with plasmids in vitro and in vivo. The expression of PTEN was detected by Western blot. The biological roles were measured by wound healing assay, transwell assay, and CCK-8 assay. Results: In the present study, we found that circSLC8A1 was down-regulated in bladder cancer tissues and cell lines, and circSLC8A1 expression was associated with the pathological stage and histological grade of bladder cancer. Over-expression of circSLC8A1 inhibited cell migration, invasion and proliferation both in vitro and in vivo. Mechanistically, circSLC8A1 could directly interact with miR-130b/miR-494, and subsequently act as a miRNA sponge to regulate the expression of the miR-130b/miR-494 target gene PTEN and downstream signaling pathway, which suppressed the progression of bladder cancer. Conclusions: CircSLC8A1 acts as a tumor suppressor by a novel circSLC8A1/miR-130b, miR-494/PTEN axis, which may provide a potential biomarker and therapeutic target for the management of bladder cancer. Background Bladder cancer is the most common malignancy of the urinary system and is one of the most prevalent malignancies worldwide [1]. In China, the mortality and morbidity of bladder cancer ranked first among all the tumors of urinary system [2]. Bladder cancer can be classified into two types according to the depth of tumor invasion: non-muscle invasive tumor (70~80%) and muscle-invasive tumor (20~30%) [3].For the patients with muscle-invasive bladder cancer, the occurrence of metastasis is more frequent, and the prognosis is poorer [4]. Even in those muscle-invasive bladder cancer patients who receive optimal treatment with surgery and chemotherapy, the 5-year overall survival rate is only 60% due to distant metastasis [5]. Therefore, it is of great clinical significance to clarify the molecular mechanisms that drive the progression of bladder cancer, which will help to develop more effective anticancer therapies. Circular RNA (circRNA) is a novel class of endogenous noncoding RNA molecules generally characterized

p300 and CREB-binding protein (CBP) are ubiquitously expressed pleiotropic lysine acetyltransferases and play a key role as transcriptional co-activators that are essential for a multitude of cellular processes. Despite great importance, there is a lack of highly selective, potent, druglike p300/CBP inhibitors. Through the artificial-intelligence-assisted drug discovery pipeline and further optimization, we reported the discovery of novel, highly selective, potent small-molecule inhibitors of p300/CBP histone acetyltransferases (HAT) with desired druglike properties, exemplified by B026. Our data demonstrated that B026, with half maximal inhibitory concentration (IC50) values of 1.8 nM to p300 and 9.5 nM to CBP enzyme inhibitory activity, is the most potent, selective p300/CBP HAT inhibitor. Moreover, B026 achieves significant and dose-dependent tumor growth inhibition in an animal model of human cancer, suggesting that B026 is a highly promising p300/CBP HAT inhibitor and warrants extensive preclinical investigation as a potential clinical development candidate.

Colorectal cancer (CRC) is a very common metastatic tumor with active angiogenesis that requires active angiogenesis. Recently, increased microRNA-181a-5p (miR-181a) expression was found to be significantly associated with liver metastasis and poor outcome in CRC patients. In this study, the role of miR-181a in tumor angiogenesis was further investigated. Capillary tube formation assays were used to demonstrate the ability of miR-181a to promote tumor angiogenesis. Bioinformatics analyses identified SRC kinase signaling inhibitor 1 (SRCIN1) as a potential target of miR-181a. Next, two CRC cell lines (HT29 and SW480) were used to clarify the function of miR-181a through SRCIN1 targeting. In addition, the biological effects of SRCIN1 inhibition by miR-181a were examined in vitro by quantitative RT-PCR, western blotting and enzyme-linked immunosorbent assay and in vivo by Matrigel plug angiogenesis assays and immunohistochemical staining. In clinical samples, Fluorescence in situ hybridization and immunofluorescence were performed to detect the relation between miR-181a and SRCIN1. In addition, SRCIN1 protein and miR-181a expression levels in CRC tissues were also measured by western blot and quantitative real-time polymerase chain reaction. MiR-181a markedly augmented the capability of CRC cells to advance tube formation in endothelial cells in vitro. The Matrigel plug assay showed that miR-181a promoted angiogenesis in vivo. In conclusion, miR-181a inhibited SRCIN1, which caused SRC to transform from an inactive status to an active conformation and to trigger vascular endothelial growth factor secretion, leading to increased angiogenesis. MiR-181a dysregulation contributes to angiogenesis in CRC, and downregulation of miR-181a represents a promising, novel strategy to achieve an efficient antiangiogenic response in anti-CRC therapy.