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MicroRNAs have been implicated in regulating diverse cellular pathways. Emerging evidence indicates that miR-143 plays causal roles in cancer tumorigenesis as a tumor suppress gene; however, its role in prostate cancer tumorigenesis remains largely unknown. The aims of this study were to verify the effect of miR-143 on proliferation and migration abilities of prostate cancer cells. The expression level of miR-143 and its target gene KRAS were measured by realtime PCR and western blotting, respectively. Effects of miR-143 in cell proliferation, migration and chemosensitivity were evaluated by MTT assay, FACS cell cycle analysis, colony formation assay, and transwell migratory assay. Our results revealed an inverse correlation of expression between miR-143 and KRAS protein in prostate cancer samples (Pearson's correlation scatter plots: R = -0.707, P < 0.05). Moreover, over-expression of miR-143 in prostate cancer cells suppressed their proliferation and migration and increased their sensitivity to docetaxel by targeting EGFR/RAS/MAPK pathway. These findings suggest that miR-143 plays an important role in prostate cancer proliferation, migration and chemosensitivity by suppressing KRAS and subsequent inactivation of MAPK pathway, which provides a potential development of a new approach for the treatment of prostate cancer.

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In nature, cells self-assemble into spatially coded tissular configurations to execute higherorder biological functions as a collective. This mechanism has stimulated the recent trend in synthetic biology to construct tissue-like assemblies from protocell entities, with the aim to understand the evolution mechanism of multicellular mechanisms, create smart materials or devices, and engineer tissue-like biomedical implant. However, the formation of spatially coded and communicating micro-architectures from large quantity of protocell entities, especially for lipid vesicle-based systems that mostly resemble cells, is still challenging. Herein, we magnetically assemble giant unilamellar vesicles (GUVs) or cells into various microstructures with spatially coded configurations and spatialized cascade biochemical reactions using a stainless steel mesh. GUVs in these tissue-like aggregates exhibit uncustomary osmotic stability that cannot be achieved by individual GUVs suspensions. This work provides a versatile and cost-effective strategy to form robust tissue-mimics and indicates a possible superiority of protocell colonies to individual protocells.

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In plants, autophagy is involved in responses to viral infection. However, the role of host factors in mediating autophagy to suppress viruses is poorly understood. A previously uncharacterized plant protein, NbP3IP, was shown to interact with p3, an RNA-silencing suppressor protein encoded by Rice stripe virus (RSV), a negative-strand RNA virus. The potential roles of NbP3IP in RSV infection were examined. NbP3IP degraded p3 through the autophagy pathway, thereby affecting the silencing suppression activity of p3. Transgenic overexpression of NbP3IP conferred resistance to RSV infection in Nicotiana benthamiana. RSV infection was promoted in ATG5-or ATG7-silenced plants and was inhibited in GAPC-silenced plants where autophagy was activated, confirming the role of autophagy in suppressing RSV infection. NbP3IP interacted with NbATG8f, indicating a potential selective autophagosomal cargo receptor role for P3IP. Additionally, the rice NbP3IP homolog (OsP3IP) also mediated p3 degradation and interacted with OsATG8b and p3. Through identification of the involvement of P3IP in the autophagy-mediated degradation of RSV p3, we reveal a new mechanism to antagonize the infection of RSV, and thereby provide the first evidence that autophagy can play an antiviral role against negative-strand RNA viruses.

Salt stress triggers the overdose accumulation of reactive oxygen species (ROS) in crop plants, leading to severe oxidative damage to living tissues. MicroRNAs (miRNAs) act as master regulators orchestrating the stress responsive regulatory networks as well as salt tolerance. However, the fundamental roles of miRNAs in modulating salt tolerance in cereal crops, especially in salt-triggered ROS scavenging remain largely unknown. Through small RNA sequencing, a salt-responsive miRNA, miR172 was identified in rice. Further, by generating the miR172-overexpression or MIR172 gene loss-of-function mutant lines, the biological significance of miR172 and its downstream signaling pathways related to salt tolerance were defined. We demonstrated that miR172 is a positive regulator of salt tolerance in both rice and wheat. More interestingly, miR172a and miR172b, but not miR172c or miR172d are involved in salt stress response, emphasizing the functional differentiation within miR172 family members. Further evidence uncovers a novel miR172/IDS1 regulatory module that functions as a crucial molecular rheostat in maintaining ROS homeostasis during salt stress, mainly through balancing the expression of a group of ROS-scavenging genes. Our findings establish a direct molecular link between miRNAs and detoxification response in cereal crops for improving salt tolerance.