In the past period, due to the rapid development of next-generation sequencing technology, accumulating evidence has clarified the complex role of the human microbiota in the development of cancer and the therapeutic response. More importantly, available evidence seems to indicate that modulating the composition of the gut microbiota to improve the efficacy of anti-cancer drugs may be feasible. However, intricate complexities exist, and a deep and comprehensive understanding of how the human microbiota interacts with cancer is critical to realize its full potential in cancer treatment. The purpose of this review is to summarize the initial clues on molecular mechanisms regarding the mutual effects between the gut microbiota and cancer development, and to highlight the relationship between gut microbes and the efficacy of immunotherapy, chemotherapy, radiation therapy and cancer surgery, which may provide insights into the formulation of individualized therapeutic strategies for cancer management. In addition, the current and emerging microbial interventions for cancer therapy as well as their clinical applications are summarized. Although many challenges remain for now, the great importance and full potential of the gut microbiota cannot be overstated for the development of individualized anti-cancer strategies, and it is necessary to explore a holistic approach that incorporates microbial modulation therapy in cancer.

Computed tomography is useful for delineation of anatomical characteristics of the nasolacrimal canal and to diagnose nasolacrimal canal malformation. Malformed nasolacrimal canals are of two main types: fundamental and special. Hydrostatic pressure in the lacrimal duct appears to the underlying mechanism as enlargement of the nasolacrimal canal in the unilateral fundamental type. [J Pediatr Ophthalmol Strabismus. 2017;54(4):238-243.].

BackgroundLong noncoding RNAs (lncRNAs) have emerged to have irreplaceable roles in the epigenetic regulation of cancer progression, but their biological functions in colorectal cancer (CRC) remain unclear.MethodsLncRNA expression profiles in CRC tissue and their normal counterpart were explored. Through gain and loss of function approaches, the role of lncRNA PTTG3P was validated in relevant CRC cells and subcutaneous tumor model. The correlations of PTTG3P expression with clinical outcomes were assessed.ResultsPTTG3P was upregulated in CRC tissues and was closely correlated with unsatisfactory prognosis. PTTG3P facilitated glycolysis and proliferation, and the transcriptional regulator YAP1 was necessary for PTTG3P-induced proliferation. Mechanistically, the N6-methyladenosine (m6A) subunit METTL3 increased PTTG3P expression by influencing its stability, while insulin-like growth factor 2 mRNA binding protein 2 (IGF2BP2) could identify PTTG3P m6A methylation status and bind to it. IGF2BP2 knockdown partly recovered PTTG3P expression induced by METTL3, indicating that METTL3-regulated PTTG3P expression depended on the presence of IGF2BP2. Finally, rescue assays validated the critical role of the METTL3/PTTG3P/YAP1 axis on CRC proliferation.ConclusionsPTTG3P is an independent prognostic biomarker for CRC. The METTL3/PTTG3P/YAP1 axis promotes the progression of CRC and is a promising treatment target.

Long noncoding RNAs (lncRNAs) play critical factors in tumor progression and are ectopically expressed in malignant tumors. Until now, lncRNA PTTG3P biological function in colorectal cancer (CRC) needs further to be clarified. qRT-PCR was used to measure the PTTG3P level and CCK-8, glucose uptake, lactate assay, ATP assay, ECAR assay, and xenograft mice model were adopted to evaluate the glycolysis and proliferation, and macrophage polarization were determined in CRC cells. Xenograft experiments were utilized to analyze tumor growth. Ectopic expression of PTTG3P was involved in CRC and related to dismal prognosis. Through gain-of-function and loss-of-function approaches, PTTG3P enhanced cell proliferation and glycolysis through YAP1. Further, LDHA knockdown or glycolysis inhibitor (2-DG,3-BG) recovered PTTG3P-induced proliferation. And PTTG3P overexpression could facilitate M2 polarization of macrophages. Silenced PTTG3P decreased the level of inflammatory cytokines TNF-α, IL-1β, and IL-6, and low PTTG3P expression related with CD8+ T, NK, and TFH cell infiltration. Besides, HIF1A could increase PTTG3P expression by binding to the PTTG3P promoter region. Hypoxia-induced PTTG3P contributes to glycolysis and M2 phenotype of macrophage, which proposes a novel approach for clinical treatment.