Extracellular vesicles (EVs), a class of heterogeneous membrane vesicles, are generally divided into exosomes and microvesicles on basis of their origination from the endosomal membrane or the plasma membrane, respectively. EV-mediated bidirectional communication among various cell types supports cancer cell growth and metastasis. EVs derived from different cell types and status have been shown to have distinct RNA profiles, comprising messenger RNAs and non-coding RNAs (ncRNAs). Recently, ncRNAs have attracted great interests in the field of EV-RNA research, and growing numbers of ncRNAs ranging from microRNAs to long ncRNAs have been investigated to reveal their specific functions and underlying mechanisms in the tumor microenvironment and premetastatic niches. Emerging evidence has indicated that EV-RNAs are essential functional cargoes in modulating hallmarks of cancers and in reciprocal crosstalk within tumor cells and between tumor and stromal cells over short and long distance, thereby regulating the initiation, development and progression of cancers. In this review, we discuss current findings regarding EV biogenesis, release and interaction with target cells as well as EV-RNA sorting, and highlight biological roles and molecular mechanisms of EV-ncRNAs in cancer biology.

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Summary1. Root and shoot competition affect plant growth in different ways, but their effects on reproductive allocation have not been investigated. If root and shoot competition affect reproductive output in a population differently, this will influence the evolution of plant populations growing under various competitive regimes. 2. We conducted a field experiment to investigate the effects of root, shoot and full competition from naturally occurring surrounding vegetation on growth and reproduction of an annual plant, Chenopodium acuminatum, under low and high soil fertility. Root competition was eliminated by inserting a PVC pipe vertically into the soil around target individuals, and shoot competition was removed by installing inverted wire cones above-ground. Plants were measured after 11 weeks of growth. The relationships between reproductive (R) and vegetative (V) biomass among treatments were compared. 3. Without fertilizer, the competitive response of target plants to root competition was greater than that to shoot competition, while in the fertilized treatment, the opposite was the case. Fertilization increased target plant size under no or root competition, but did not affect mean plant size for individuals experiencing shoot or full competition. Variation in size among target plants was highest under shoot competition at high fertility. 4. The slope of log R-log V relationship under fertilized conditions was significantly higher than without fertilizer addition. The slope was higher under shoot and full competition than under root or no competition at both fertility levels. There were many more small individuals when competition was for light than for soil resources. These small individuals developed more slowly and had fewer flowering branches and lower reproductive allocation at harvest than large individuals. 5. Synthesis. Our results demonstrated that shoot competition affects the observed pattern of reproductive allometry among individuals in the field, and this has implications for the fitness of competing plants. The steeper log R-log V slope of populations competing above-ground may intensify the role of directional selection under light competition, making the effects of shoot competition more important than those of root competition for the evolution of weeds in fertile environments.

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Renal cell carcinoma (RCC) is the most common form of kidney cancer, with a high recurrence rate and metastasis capacity. Circular RNAs (circRNAs) have been suggested to act as the critical regulator in several diseases. This study is designed to investigate the role of circCSNK1G3 on RCC progression. We observed a highly expression of circCSNK1G3 in RCC tissues compared with normal tissues. The aberrantly circCSNK1G3 promoted the tumour growth and metastasis in RCC. In the subsequent mechanism investigation, we discovered that the tumour‐promoting effects of circCSNK1G3 were, at least partly, achieved by up‐regulating miR‐181b. Increased miR‐181b inhibits several tumour suppressor gene, including CYLD, LATS2, NDRG2 and TIMP3. Furthermore, the decreased TIMP3 leads to the enhanced epithelial to mesenchymal transition (EMT) process, thus promoting the cancer metastasis. In conclusion, we identified the oncogenic role of circCSNK1G3 in RCC progression and demonstrated the regulatory role of circCSNK1G3 induced miR‐181b expression, which leads to TIMP3‐mediated EMT process, thus resulting in tumour growth and metastasis in RCC. This study reveals the promise of circCSNK1G3 to be developed as a potential diagnostic and prognostic biomarker in the clinic. And the roles of circCSNK1G3 in cancer research deserve further investigation.