Identification of an efficient phenanthrene-degrading Pseudarthrobacter sp. L1SW and characterization of its metabolites and catabolic pathway.

Phenanthrene, a typical chemical of polycyclic aromatic hydrocarbons (PAHs) pollutants, severely threatens health of wild life and human being. Microbial degradation is effective and environment-friendly for PAH removal, while the phenanthrene-degrading mechanism in Gram-positive bacteria is unclear. In this work, one Gram-positive strain of plant growth-promoting rhizobacteria (PGPR), Pseudarthrobacter sp. L1SW, was isolated and identified with high phenanthrene-degrading efficiency and great stress tolerance. It degraded 96.3% of 500 mg/L phenanthrene in 72 h and kept stable degradation performance with heavy metals (65 mg/L of Zn2+, 5.56 mg/L of Ni2+, and 5.20 mg/L of Cr3+) and surfactant (10 CMC of Tween 80). Strain L1SW degraded phenanthrene mainly through phthalic acid pathway, generating intermediate metabolites including cis-3,4-dihydrophenanthrene-3,4-diol, 1-hydroxy-2-naphthoic acid, and phthalic acid. A novel metabolite (m/z 419.0939) was successfully separated and identified as an end-product of phenanthrene, suggesting a unique metabolic pathway. With the whole genome sequence alignment and comparative genomic analysis, 19 putative genes associated with phenanthrene metabolism in strain L1SW were identified to be distributed in three gene clusters and induced by phenanthrene and its metabolites. These findings advance the phenanthrene-degrading study in Gram-positive bacteria and promote the practical use of PGPR strains in the bioremediation of PAH-contaminated environments.

RP11-296E3.2 acts as an important molecular chaperone for YBX1 and promotes colorectal cancer proliferation and metastasis by activating STAT3.

BACKGROUND: RP11-296E3.2 is a novel long noncoding RNA (lncRNA) associated with colorectal cancer (CRC) metastasis, that was reported in our previous clinical studies. However, the mechanisms of RP11-296E3.2 in colorectal tumorigenesis remain elusive. METHODS: RNA sequencing (RNA-seq), Fluorescence in situ hybridization (FISH), Transwell assays and others, were performed to evaluate the function of RP11-296E3.2 for proliferation and metastasis in vitro. In situ and metastatic tumor models were performed to evaluate the function of RP11-296E3.2 for proliferation and metastasis in vivo. RNA-pulldown, RNA-interacting protein immunoprecipitation (RIP), tissue microarray (TMA) assay, a luciferase reporter assay, chromatin immunoprecipitation (ChIP) and others were performed to explore the mechanisms by which RP11-296E3.2 regulates CRC tumorigenesis. RESULTS: RP11-296E3.2 was confirmed to be associated with CRC cell proliferation and metastasis in vitro and in vivo. Mechanistically, RP11-296E3.2 directly bound to recombinant Y-Box Binding Protein 1 (YBX1) and enhanced signal transducer and activator of transcription 3 (STAT3) transcription and phosphorylation. YBX1 promoted the CRC cell proliferation and migration, while knockdown of RP11-296E3.2 attenuated the effects of YBX1 on CRC cell proliferation, and metastasis and the expression of several related downstream genes. We are the first to discover and confirm the existence of the YBX1/STAT3 pathway, a pathway dependent on RP11-296E3.2. CONCLUSION: Together, these novel findings show that the RP11-296E3.2/YBX1 pathway promotes colorectal tumorigenesis and progression by activating STAT3 transcription and phosphorylation, and suggest that RP11-296E3.2 is a potential diagnostic biomarker and therapeutic target in CRC.