Significance We demonstrate, to our knowledge for the first time, that bacterial biofilms are associated with colorectal cancers, one of the leading malignancies in the United States and abroad. Colon biofilms, dense communities of bacteria encased in a likely complex matrix that contact the colon epithelial cells, are nearly universal on right colon tumors. Most remarkably, biofilm presence correlates with bacterial tissue invasion and changes in tissue biology with enhanced cellular proliferation, a basic feature of oncogenic transformation occurring even in colons without evidence of cancer. Microbiome profiling revealed that biofilm communities on paired normal mucosa cluster with tumor microbiomes but lack distinct taxa differences. This work introduces a previously unidentified concept whereby microbial community structural organization exhibits the potential to contribute to disease progression.

Circular RNAs (circRNAs), a novel class of long noncoding RNAs, are characterized by a covalently closed continuous loop without 5′ or 3′ polarities structure and have been widely found in thousands of lives including plants, animals and human beings. Utilizing the high-throughput RNA sequencing (RNA-seq) technology, recent findings have indicated thata great deal of circRNAs, which are endogenous, stable, widely expressed in mammalian cells, often exhibit cell type-specific, tissue-specific or developmental-stage-specific expression. Evidences are arising that some circRNAs might regulate microRNA (miRNA) function as microRNA sponges and play a significant role in transcriptional control. circRNAs associate with related miRNAs and the circRNA-miRNA axes are involved in a serious of disease pathways such as apoptosis, vascularization, invasion and metastasis. In this review, we generalize and analyse the aspects including synthesis, characteristics, classification, and several regulatory functions of circRNAs and highlight the association between circRNAs dysregulation by circRNA-miRNA-mRNA axis and sorts of diseases including cancer- related and non-cancer diseases.”

Summary Pro-carcinogenic bacteria have the potential to initiate and/or promote colon cancer, in part via immune mechanisms that are incompletely understood. Using ApcMin mice colonized with the human pathobiont enterotoxigenic Bacteroides fragilis (ETBF) as a model of microbial-induced colon tumorigenesis, we show that the Bacteroides fragilis toxin (BFT) triggers a pro-carcinogenic multi-step inflammatory cascade requiring IL-17R, NF-κB, and Stat3 signaling in colonic epithelial cells (CECs). Although necessary, Stat3 activation in CECs is not sufficient to trigger ETBF colon tumorigenesis. Notably, IL-17-dependent NF-κB activation in CECs induces a proximal to distal mucosal gradient of C-X-C chemokines, including CXCL1 that mediates the recruitment of CXCR2-expressing polymorphonuclear immature myeloid cells with parallel onset of ETBF-mediated distal colon tumorigenesis. Thus, BFT induces a procarcinogenic signaling relay from the CEC to a mucosal Th17 response that results in NFκB activation selectively in distal colon CECs, that collectively triggers myeloid cell-dependent distal colon tumorigenesis.

CircRNA expression profiles for gastric cancer (GC) were screened using plasma samples from 10 GC patients with different TNM stages and 5 healthy individuals as controls. Results showed lower expression of circ-KIAA1244 in GC tissues, plasmas, and cells compare to normal controls. Further clinical data analysis demonstrated that a decreased expression of circ-KIAA1244 in plasmas was negatively correlated with TNM stage and lymphatic metastasis, and a shorter overall survival time of GC patients. Moreover, we found that circ-KIAA1244 could be detected in GC plasma exosomes and showed no obvious significance compared to the expression level in the corresponding plasmas. This study revealed a GC-tissues-derived circ-KIAA1244 could serve a novel circulating biomarker for detection of GC.Electronic supplementary materialThe online version of this article (10.1186/s12943-018-0888-8) contains supplementary material, which is available to authorized users.