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Fusobacterium nucleatum Reducing METTL3-mediated m6A Modification Contributes to Colorectal Cancer Aggressiveness [RNA-Seq]

ABSTRACT: Transcriptome profiling revealed that KIF26B was associated with cell-cell junction and response to growth factor stimulation, which are important for CRC cell aggressiveness. And gene set enrichment analysis suggested that Hippo signaling pathway was significantly enriched in KIF26B-regulated gene signatures

ORGANISM(S): Homo sapiens

PROVIDER: GSE150309 | GEO | 2022/02/07

REPOSITORIES: GEO

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Fusobacterium nucleatum Reducing METTL3-mediated m6A Modification Contributes to Colorectal Cancer Aggressiveness

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-02-08 | GSE150310 | GEO

Fusobacterium nucleatum Reducing METTL3-mediated m6A Modification Contributes to Colorectal Cancer Aggressiveness [RIP-Seq]

Project description:To investigate the role of Fusobacterium nucleatum-mediated m6A modification, we performed m6A-sequencing to map the m6A modification in control or Fusobacterium nucleatum-treated HCT116 cells.

2022-02-07 | GSE150308 | GEO

Fusobacterium nucleatum Reducing METTL3-mediated m6A Modification Contributes to Colorectal Cancer Aggressiveness

Project description:Fusobacterium nucleatum Reducing METTL3-mediated m6A Modification Contributes to Colorectal Cancer Aggressiveness

| PRJNA631745 | ENA

Fusobacterium nucleatum Reducing METTL3-mediated m6A Modification Contributes to Colorectal Cancer Aggressiveness [RIP-Seq]

Project description:Fusobacterium nucleatum Reducing METTL3-mediated m6A Modification Contributes to Colorectal Cancer Aggressiveness [RIP-Seq]

| PRJNA631748 | ENA

Fusobacterium nucleatum Reducing METTL3-mediated m6A Modification Contributes to Colorectal Cancer Aggressiveness [RNA-Seq]

Project description:Fusobacterium nucleatum Reducing METTL3-mediated m6A Modification Contributes to Colorectal Cancer Aggressiveness [RNA-Seq]

| PRJNA631749 | ENA

Fusobacterium nucleatum reduces METTL3-mediated m<sup>6</sup>A modification and contributes to colorectal cancer metastasis.

Project description:Microbiota-host interactions play critical roles in colorectal cancer (CRC) progression, however, the underlying mechanisms remain elusive. Here, we uncover that Fusobacterium nucleatum (F. nucleatum) induces a dramatic decline of m6A modifications in CRC cells and patient-derived xenograft (PDX) tissues by downregulation of an m6A methyltransferase METTL3, contributing to inducation of CRC aggressiveness. Mechanistically, we characterized forkhead box D3 (FOXD3) as a transcription factor for METTL3. F. nucleatum activates YAP signaling, inhibits FOXD3 expression, and subsequently reduces METTL3 transcription. Downregulation of METTL3 promotes its target kinesin family member 26B (KIF26B) expression by reducing its m6A levels and diminishing YTHDF2-dependent mRNA degradation, which contributes to F. nucleatum-induced CRC metastasis. Moreover, METTL3 expression is negatively correlated with F. nucleatum and KIF26B levels in CRC tissues. A high expression of KIF26B is also significantly correlated with a shorter survival time of CRC patients. Together, our findings provide insights into modulating human m6A epitranscriptome by gut microbiota, and its significance in CRC progression.

| S-EPMC8913623 | biostudies-literature

Intracellular Fusobacterium nucleatum infection increases METTL3-mediated m6A methylation to promote the metastasis of esophageal squamous cell carcinoma.

Project description:IntroductionThe tumor-associated microbiota plays a vital role in cancer development. Accumulating evidence shows that Fusobacterium nucleatum (Fn) participates in the progression of multiple tumor types. However, the underlying mechanisms remain unclear.ObjectivesThis study examined the expression of methyltransferase-like protein 3 (METTL3) during Fn infection and elucidated the function and pathway of Fn-induced m6A methylation in esophageal squamous cell carcinoma (ESCC).MethodsThe abundance of Fn in patient tissues was determined by qPCR. Western blot, qRT-PCR, and immunohistochemistry were performed to measure METTL3 expression in cells and tissues. METTL3 function was evaluated in vitro by colony formation and cell migration assays. MeRIP-qPCR was performed to determine the relationship between METTL3 and c-Myc. In addition, the half-lives of genes that are downstream of METTL3 were determined with RNA stability assays.ResultsFn was enriched in hepatocellular carcinoma (HCC), breast cancer (BRCA), ESCC, and colorectal cancer (CRC) tumor tissues. METTL3 expression was positively associated with Fn abundance in ESCC tissues. Fn could survive and proliferation as well as increase METTL3 expression in ESCC, HCC, CRC, and BRCA cells. Moreover, METTL3 overexpression promoted ESCC cells proliferation, migration in vivo and in vitro. Mechanistically, Intracellular Fn infection increases METTL3 transcription. METTL3 promoted c-Myc mRNA methylation in the 3'-untranslated Region (3'-UTR) and enhanced its mRNA stability in a YTH N6-Methyladenosine RNA binding protein 1(YTHDF1)-dependent manner, which contributes to Fn induced ESCC proliferation and metastasis.ConclusionsThis study indicates that intracellular Fn infection promotes ESCC development and metastasis, and eradicating Fn infection may be a promising strategy for treating ESCC.

| S-EPMC11258656 | biostudies-literature

Fusobacterium nucleatum-positive colorectal cancer.

Project description:Colorectal cancer (CRC) is an important threat to human health and the fourth leading cause of mortality worldwide. Accumulating evidence indicates that the composition of the intestinal flora is associated with the occurrence of CRC. Fusobacterium nucleatum (Fn), one of the highly enriched bacteria in CRC tissues, invades the mucosa with adhesion factors and virulence proteins, interacts with the host immune system and promotes the occurrence and development of CRC and chemoresistance. Fn infection is prevalent in human colorectal carcinoma, although the infection rate varies in different regions. Fn may be used as a prognostic indicator of CRC. It is important to understand the multi-pathway carcinogenic mechanisms associated with CRC in order to develop novel antibacterial drugs against Fn. The current review summarizes the role of Fn and relevant research concerning CRC published in recent years, focusing on Fn infection in CRC, pathogenesis of Fn, Fn-positive CRC treatment, screening and prevention strategies against Fn-positive CRC.

| S-EPMC6607099 | biostudies-literature

Autoaggregation response of Fusobacterium nucleatum.

Project description:Fusobacterium nucleatum is a gram-negative oral bacterial species associated with periodontal disease progression. This species is perhaps best known for its ability to adhere to a vast array of other bacteria and eukaryotic cells. Numerous studies of F. nucleatum have examined various coaggregation partners and inhibitors, but it is largely unknown whether these interactions induce a particular genetic response. We tested coaggregation between F. nucleatum ATCC strain 25586 and various species of Streptococcus in the presence of a semidefined growth medium containing saliva. We found that this condition could support efficient coaggregation but, surprisingly, also stimulated a similar degree of autoaggregation. We further characterized the autoaggregation response, since few reports have examined this in F. nucleatum. After screening several common coaggregation inhibitors, we identified l-lysine as a competitive inhibitor of autoaggregation. We performed a microarray analysis of the planktonic versus autoaggregated cells and found nearly 100 genes that were affected after only about 60 min of aggregation. We tested a subset of these genes via real-time reverse transcription-PCR and confirmed the validity of the microarray results. Some of these genes were also found to be inducible in cell pellets created by centrifugation. Based upon these data, it appears that autoaggregation activates a genetic program that may be utilized for growth in a high cell density environment, such as the oral biofilm.

| S-EPMC2794088 | biostudies-literature

Comparative Genome Analysis of Fusobacterium nucleatum.

Project description:Fusobacterium nucleatum is considered to be a key oral bacterium in recruiting periodontal pathogens into subgingival dental plaque. Currently F. nucleatum can be subdivided into five subspecies. Our previous genome analysis of F. nucleatum W1481 (referred to hereafter as W1481), isolated from an 8-mm periodontal pocket in a patient with chronic periodontitis, suggested the possibility of a new subspecies. To further investigate the biology and relationships of this possible subspecies with other known subspecies, we performed comparative analysis between W1481 and 35 genome sequences represented by the five known Fusobacterium subspecies. Our analyses suggest that W1481 is most likely a new F. nucleatum subspecies, supported by evidence from phylogenetic analyses and maximal unique match indices (MUMi). Interestingly, we found a horizontally transferred W1481-specific genomic island harboring the tripartite ATP-independent (TRAP)-like transporter genes, suggesting this bacterium might have a high-affinity transport system for the C4-dicarboxylates malate, succinate, and fumarate. Moreover, we found virulence genes in the W1481 genome that may provide a strong defense mechanism which might enable it to colonize and survive within the host by evading immune surveillance. This comparative study provides better understanding of F. nucleatum and the basis for future functional work on this important pathogen.

| S-EPMC5630926 | biostudies-literature

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