Integration analysis of transcriptome and proteome profiles brings new insights of somatic embryogenesis of two eucalyptus species.

BACKGROUND: Somatic embryogenesis (SE) is recognized as a promising technology for plant vegetative propagation. Although previous studies have identified some key regulators involved in the SE process in plant, our knowledge about the molecular changes in the SE process and key regulators associated with high embryogenic potential is still poor, especially in the important fiber and energy source tree - eucalyptus. RESULTS: In this study, we analyzed the transcriptome and proteome profiles of E. camaldulensis (with high embryogenic potential) and E. grandis x urophylla (with low embryogenic potential) in SE process: callus induction and development. A total of 12,121 differentially expressed genes (DEGs) and 3,922 differentially expressed proteins (DEPs) were identified in the SE of the two eucalyptus species. Integration analysis identified 1,353 (131 to 546) DEGs/DEPs shared by the two eucalyptus species in the SE process, including 142, 13 and 186 DEGs/DEPs commonly upregulated in the callus induction, maturation and development, respectively. Further, we found that the trihelix transcription factor ASR3 isoform X2 was commonly upregulated in the callus induction of the two eucalyptus species. The SOX30 and WRKY40 TFs were specifically upregulated in the callus induction of E. camaldulensis. Three TFs (bHLH62, bHLH35 isoform X2, RAP2-1) were specifically downregulated in the callus induction of E. grandis x urophylla. WGCNA identified 125 and 26 genes/proteins with high correlation (Pearson correlation > 0.8 or < -0.8) with ASR3 TF in the SE of E. camaldulensis and E. grandis x urophylla, respectively. The potential target gene expression patterns of ASR3 TF were then validated using qRT-PCR in the material. CONCLUSIONS: This is the first time to integrate multiple omics technologies to study the SE of eucalyptus. The findings will enhance our understanding of molecular regulation mechanisms of SE in eucalyptus. The output will also benefit the eucalyptus breeding program.

Tuning of Molecular Interactions between Zein and Tannic Acid to Modify Sunflower Sporopollenin Exine Capsules: Enhanced Stability and Targeted Delivery of Bioactive Macromolecules.

There are multiple obstacles for the storage and digestion of orally administered bioactive macromolecules. This study developed a low-cost and sustained-release delivery system (sporopollenin exine capsules with zein/tannic acid modification) of proteins with excellent storage stability, and at the same time provided insights into the sustained-release mechanism through exploring the interaction between zein and tannic acid (TA). ß-Galactosidase (ß-Gal) was utilized as a model protein and loaded into sporopollenin exine capsules (SECs), which were then coated with the zein/TA system. Under the optimized zein/TA conditions, the zein/TA system showed better performance than the zein alone system in the sustained release of ß-Gal, with the residual activity of about 70.26% after 24 h of simulated digestion. Evaluation of the storage stability demonstrated a ß-Gal residual activity of nearly 90% for 28 days at 25 °C. Additionally, FTIR analysis demonstrated that the stability of the zein/TA system depends on both hydrogen bonding and certain covalent bonding through the Schiff-base reaction, and the sustained release is regulated by the bonding strength.

Designable Carboxymethylpachymaran/Metal Ion Architecture on Sunflower Sporopollenin Exine Capsules as Delivery Vehicles for Bioactive Macromolecules.

There are multiple obstacles in the gastrointestinal tract (GIT) for oral administration of bioactive macromolecules. Here, we engineered an oral delivery vehicle (sporopollenin exine capsules with carboxymethylpachymaran (CMP)/metal ion modification) with targeted release based on food-grade ingredients and processing operations. Then, the interaction and binding mechanisms between CMP and metal ions in the vehicle were investigated. By using ß-galactosidase (ß-Gal) as a model protein, the systems were characterized for the surface morphology and monitored by the in vitro release profile of ß-Gal. Notably, the CMP/metal ion systems not only markedly decreased the CMP dosage but also achieved a valid long-term release compared with the previously reported CMP system. Among all the systems, the CMP/3% AlCl3 system showed the best ability to control the release with the maximum residual activity of ß-Gal at nearly 72% after 24 h of treatment. Subsequently, the interaction mechanism between CMP and metal ions within the system was characterized by the perspectives of microstructure, rheological properties, and spectroscopy characteristics. The results indicated that the low pH conditions are conducive to the further cross-linking of CMP and metal ions, resulting in a high gel strength and thus a dense structure, which can impact the controlled release of ß-Gal in the GIT. Overall, the system may be utilized in the administration of medical and functional foods, specifically for the delivery of bioactive proteins via the oral route.

Carboxymethylpachymaran-zein coated plant microcapsules-based ß-galactosidase encapsulation system for long-term effective delivery.

Oral delivery of ß-galactosidase (ß-Gal) for alleviating lactose intolerance is a challenge due to its degradation in the harsh gastrointestinal tract (GIT). In this study, sunflower sporopollenin exine capsules (SECs)-based systems were fabricated to serve as protective microcapsules in order to improve the stability as well as to impact the pH-responsive release of ß-Gal in GIT. The SECs extraction and loading process were optimized with the maximum residual activity of 82.75 ± 2.16%. Furthermore, the comparison of two systems indicated that ß-Gal loaded into SECs which were entrapped in CMP-zein system was superior to that in zein system in terms of delivering ß-Gal to the intestinal tract. Additionally, the interaction between CMP and zein confirmed by FTIR might contribute to the increased resistance to the GIT. Collectively, these results suggested that SECs-based CMP-zein system might be useful for encapsulation, protection, and delivery of bioactive substances.

MeCP2 triggers diabetic cardiomyopathy and cardiac fibroblast proliferation by inhibiting RASSF1A.

Diabetes causes cardiomyopathy and increases the risk of heart failure independent of hypertension and cardiac fibrosis disease. However, the molecular mechanism of cardiomyopathy caused by diabetic (DCM) is currently unknown. Here we explore the role of the Methyl CpG binding protein 2 (MeCP2) in DCM patients and a type 1 DM (T1DM) rat model. In this study, we employed streptozotocin (STZ)-induced rats DCM and DCM patient and found that MeCP2 triggers cardiac fibroblast proliferation in DCM by inhibiting of RASSF1A expression. Moreover, the in vitro study demonstrated that high glucose inhibited RASSF1A expression, accompanied by the increases of MeCP2 expression and DNA hypermethylation in RASSF1A promoter region. MeCP2 inhibition or knockdown reversed the decrease of RASSF1A transcription induced by high glucose in cardiac fibroblasts. MeCP2 triggers cardiac fibroblasts proliferation through the activation of RASSF1A/ERK1/2 signaling pathways. Our results demonstrated that MeCP2 plays a key role in RASSF1A mediated ERK1/2 activation in DCM. Taken together, these indicate that MeCP2 acts as a key regulator of DCM and cardiac fibroblasts proliferation.

Carboxymethylpachymaran entrapped plant-based hollow microcapsules for delivery and stabilization of ß-galactosidase.

ß-Galactosidase (ß-Gal) as a dietary supplement can alleviate symptoms of lactose intolerance. However, ß-Gal is deactivated due to the highly acidic conditions and proteases in the digestive tract. In this work, ß-Gal was encapsulated into L. clavatum sporopollenin exine capsules (SECs) to fabricate an oral-controlled release system and increase the stability of ß-Gal in the digestive tract. The SEC extraction process was optimized. A 3-hour vacuum loading was determined as the optimal loading time. Five different initial ratios of SECs : ß-Gal were optimized with the maximum enzyme retention rate reaching 79.40 ± 1.96%. Furthermore, ß-Gal-loaded SECs entrapped in carboxymethylpachymaran (CMP) could control the release of ß-Gal under simulated gastrointestinal conditions (SGC). The optimal enzyme retention rate reached 65.33 ± 1.46% within 24 h under SGC. Collectively, these results indicated that the entrapped SECs could be used as an effective oral delivery vehicle of ß-Gal to improve its performance as a dietary supplement in the digestion of lactose.

Oligosaccharides act as the high efficiency stabilizer for ß-galactosidase under heat treatment.

ß-Galactosidase (ß-Gal) as dietary supplement has the ability to alleviate symptoms of lactose intolerance. This study investigated the ability of oligosaccharides to protect ß-Gal against heat stress. Four kinds of oligosaccharides including Isomalto-oligosaccharides (IMO), Xylo-oligosaccharides (XOS), Konjac-oligosaccharides (KOS), and Mycose significantly increased the activity retention of ß-Gal under heat treatment. The results of three assays including circular dichroism, fluorescence, and Fourier transform infrared spectroscopy (FTIR) illustrated that these oligosaccharides could stabilize the secondary and tertiary structure of ß-Gal under thermal conditions through hydrogen bond interaction. Unlike these four oligosaccharides, Chito-oligosaccharides (COS) changed the secondary and tertiary structure of ß-Gal, thus decreasing its activity retention rate. Under heat treatment, the activity retention rate of ß-Gal with optimal composition (30% IMO, w/v and 40% XOS, w/v) reached 82.1%, which was significantly higher than that of the native ß-Gal (the activity retention rate of 20%). This study provides an insight into the mechanism by which sugar stabilizes protein under heat stress and offers guidance for application of liquid lactase to food industry.

Impact of plant extract on the gastrointestinal fate of nutraceutical-loaded nanoemulsions: phytic acid inhibits lipid digestion but enhances curcumin bioaccessibility.

The impact of phytic acid on lipid digestion and curcumin bioaccessibility in oil-in-water nanoemulsions was investigated using a simulated gastrointestinal tract (GIT). The size, charge, and structural organization of the colloidal particles in the system were measured as the curcumin-loaded emulsions (7 mg curcumin per g lipid) were passed through simulated mouth (pH 6.8, 2 min), stomach (pH 2.5, 2 hours), and small intestine (pH 7.0, 2 hours) stages. After the small intestine stage, the level of free fatty acids (FFAs) generated and the bioaccessibility of curcumin were measured. The total amount of FFAs released significantly decreased with increasing phytic acid level, from 105.7 ± 5.9% (control) to 78.4 ± 6.4% (0.5% phytic acid). Conversely, curcumin bioaccessibility significantly increased from 39.4 ± 3.5% (control) to 74.7 ± 2.6% (0.5% phytic acid). The inverse relationship between lipolysis and curcumin bioaccessibility was ascribed to the impact of phytic acid on droplet flocculation and the level of free calcium ions present, which affected the production of mixed micelles capable of solubilizing the nutraceutical. The knowledge obtained here might prove beneficial for the employment of phytic acid as a multifunctional ingredient that inhibits lipid digestion while boosting nutraceutical bioavailability.

[Research and Application of the Technical Method for the Compilation of VOCs Emission Inventories from Architectural Coatings in Beijing].

VOCs(volatile organic compounds) are important precursors of ozone and secondary organic aerosols in the atmosphere, which increase atmospheric oxidation, creating pollutants such as photochemical smog, fine particulate matter and so on. This study documented information about architectural coating VOC emission characteristics to facilitate formulation of control strategies by environmental management departments. This research was based on measured data for architectural wall and waterproof coatings to identify localized emission factors, used industry research to compile additional information, and was combined with the Beijing completed building inventory, to develop a compilation method for VOC emissions from architectural coatings. According to the above research to estimate VOC emissions of the interior wall, exterior wall and waterproof coatings in 2015, analysis of the spatial distribution of VOCs was performed and VOC emissions were estimated under two conditions regarding whether to limit the content of hazardous substances in architectural coatings from 2002-2015. The results show that ①VOC emissions from the Beijing architechtural wall and waterproof coating was about 6914.2t·a-1 in 2015. The emissions from wall paint and waterproof coating were 2394.9 t·a-1and 4519.3 t·a-1, accounting for 34.6% and 65.4%, respectively. ②The spatial distribution of VOC emissions showed that emissions were mainly concentrated around the new cities being developed in the Chaoyang and Tongzhou districts. The district with the highest VOC emission is Tongzhou District, where the proportion of emission is about 13.2%. Following it are the Changping and Chaoyang districts, respectively, at 11.8% and 10.5%. ③In 2015, because of implementation of the standards < Indoor decorating and refurbishing materials-Limit of harmful substances of interior architectural coatings > (GB 18582-2008) and < Limit of harmful substances of exterior wall coatings > (GB 24408-2009), compared to the no control scenario, the VOCs emissions under control scenario was one where VOCs emissions were reduced by 8954.2 t. ④It follows that environmental management and control of the hazardous substance contents of architectural coatings can effectively control the VOC emission in China.

[Content Levels and Compositions Characteristics of Volatile Organic Compounds(VOCs) Emission from Architectural Coatings Based on Actual Measurement].

The content levels and composition characteristics of Volatile Organic Compounds (VOCs) from architectural coatings including interior wall coatings, exterior wall coatings, waterproofing coatings, anticorrosive coatings and floor coatings were investigated in this study. Architectural coating samples were obtained from manufacturers and retail outlets and the associated VOC contents and compositions were determined based on the domestic standard methods for measurement of VOCs in architectural coatings.The results showed that the VOC contents were 0-145 g·L-1 and 0-171 g·L-1 for interior and exterior wall coatings respectively. The proportion of samples that met the standards of HJ 2537-2014 were 90%, 80%, 96% and 94% for interior wall finishing coats, interior wall primary coats, exterior wall finishing coats and exterior wall primary coats respectively.The VOC content was found to be less than 10 g·L-1 for more than 90% of polymer-cement based waterproof coatings and acrylate polymer emulsion waterproof coatings respectively, and 1-324 g·L-1 for polyurethane waterproof coatings. The VOC contents for solvent-based coatings were found to be generally high, with VOC contents ranging from between 291-681 g·L-1 and 16-580 g·L-1 for solvent-based anticorrosive coatings and solvent-based floor coatings respectively, with great variation shown between different compositions and brands. The 1,2-propanediol and ethylene glycol were the most VOC in water-based coatings with methanol and 2-amino-2-methyl-1-propanol equal second. The main VOCs in solvent-based coatings were toluene, ethyl benzene, xylenes (total), ethyl acetate, butyl acetate and isobutyl acetate.

Pathological bases and clinical impact of long noncoding RNAs in prostate cancer: a new budding star.

Long non-coding RNAs (lncRNAs) are functional RNAs longer than 200 nucleotides. Recent advances in the non-protein coding part of human genome analysis have discovered extensive transcription of large RNA transcripts that lack coding protein function, termed non-coding RNA (ncRNA). It is becoming evident that lncRNAs may be an important class of pervasive genes involved in carcinogenesis and metastasis. However, the biological and molecular mechanisms of lncRNAs in diverse diseases are not yet fully understood. Thus, it is anticipated that more efforts should be made to clarify the lncRNA world. Moreover, accumulating evidence has demonstrated that many lncRNAs are dysregulated in prostate cancer (PC) and closely related to tumorigenesis, metastasis, and prognosis or diagnosis. In this review, we will briefly outline the regulation and functional role of lncRNAs in PC. Finally, we discussed the potential of lncRNAs as prospective novel targets in PC treatment and biomarkers for PC diagnosis.

Engineering Multifunctional Coatings on Nanoparticles Based on Oxidative Coupling Assembly of Polyphenols for Stimuli-Responsive Drug Delivery.

In this study, zein nanoparticles (NPs) with novel multifunctional coatings based on oxidative coupling assembly of polyphenols were synthesized for the first time. This coating was formed by oxidative self-polymerization of the organic ligands (polyphenols) in an alkaline condition, which could be biodegraded by acidic pH, as a result, impacting the pH-responsive property of the system. More importantly, the high level of intracellular glutathione (GSH) could induce the biodegradation of the polyphenol coatings, resulting in a fast release of trapped anticancer drugs in the cells. Based on confocal laser scanning microscopy (CLSM) and cytotoxicity experiments, drug-loaded and polyphenol-coated zein NPs were shown to possess highly efficient internalization and an apparent cytotoxic effect on HeLa cells. Notably, the CLSM observation illustrated that coated zein NPs showed delayed drug release compared with free drug or DOX-loaded zein NPs without coatings, resulting from the pH-responsive release of loaded drug in the extra/intracellular environment. Additionally, the short-time cytotoxicity and morphology observation also confirmed the delayed drug release behavior of coated NPs. These highly biocompatible and biodegradable polyphenol-coated zein NPs may be promising vectors in the field of controlled-release biomedical applications and cancer therapy.

LncRNA GAS5 controls cardiac fibroblast activation and fibrosis by targeting miR-21 via PTEN/MMP-2 signaling pathway.

Long noncoding RNAs (LncRNAs) are aberrantly expressed in many diseases including cardiac fibrosis. LncRNA growth arrest-specific 5 (GAS5) is reported as a significant mediator in the control of cell proliferation and growth; however, the role and function in cardiac fibrosis remain unknown. In this study, we confirmed that GAS5 was lowly expressed in cardiac fibrosis tissues as well as activated cardiac fibroblast. Overexpression of GAS5 inhibited the proliferation of cardiac fibroblast. Moreover, microRNA-21 (miR-21) has been reported to be overexpressed in cardiac fibrosis tissues as well as activated cardiac fibroblast, which is responsible for the progression of cardiac fibrosis. We found that up-regulated GAS5 decreased the expression of miR-21 significantly. Furthermore, GAS5 that upregulated or downregulated the expression of PTEN through miR-21 in cardiac fibroblasts. Taken together, GAS5 plays a suppressive role in cardiac fibrosis via negative regulation of miR-21. These results indicated that GAS5 may be a novel therapeutic target for further research of cardiac fibrosis.

Repression of TSC1/TSC2 mediated by MeCP2 regulates human embryo lung fibroblast cell differentiation and proliferation.

Pulmonary fibrosis (PF) is a severe inflammatory disease with limited effective treatments. It is known that the transdifferentiation of human embryo lung fibroblast (HELF) cells from pulmonary fibroblasts into myofibroblasts, contributes to the progression of pulmonary fibrogenesis. The tuberous sclerosis proteins TSC1 and TSC2 are two key signaling factors which can suppress cell growth and proliferation. However, the roles of TSC1 and TSC2 in lung fibroblast are unclear. Here, we developed a PF model with bleomycin (BLM) in mice and conducted several simulation experiments in HELF cells. Our study shows that the expression of TSC1 and TSC2 in fibrotic mice lung was reduced and stimulation of HELF cells with TGF-ß1 resulted in a down-regulation of TSC1 and TSC2. In addition, overexpression of TSC1 or TSC2 decreased cell proliferation and differentiation. Furthermore, we found that reduced expression of TSC1 and TSC2 caused by TGF-ß1 is associated with the promoter methylation status of TSC1 and TSC2. MeCP2, controls an epigenetic pathway that promotes myofibroblast transdifferentiation and fibrosis. We found that expression of TSC1 and TSC2 can be repressed by MeCP2, which regulates HELF cell differentiation and proliferation as myofibroblasts and lead to PF ultimately.

miR-200a controls hepatic stellate cell activation and fibrosis via SIRT1/Notch1 signal pathway.

OBJECTIVES: miR-200a has been established as a key regulator of HSC activation processes in liver fibrosis. Epigenetic silencing of miR-200a contributing to SIRT1 over-expression has been discussed in breast cancer; however, whether miR-200a controls SIRT1 gene expression in hepatic fibrosis is still unknown. METHODS AND MATERIALS: We analyzed miR-200a regulation of SIRT1 expression in CCl4-induced liver fibrosis and TGF-ß1-mediated activation of HSC. miR-200a, SIRT1, α-SMA, Col1A1, Notch1 and NICD expression were estimated by Western blotting, qRT-PCR and Immunohistochemistry. HSCs were transfected with miR-200a mimic, miR-200a inhibitor and SIRT1-RNAi. Luciferase reporter assays further confirmed the interaction between miR-200a and the SIRT1 mRNA 3'-UTR. Cell proliferation ability was assessed by MTT and cell cycle. RESULTS: We found that treatment activated HSC with miR-200a mimics, restored miR-200a expression and reduced SIRT1 levels. Conversely, treatment activated HSC with miR-200a inhibitors, decreased miR-200a expression and up-regulated SIRT1 levels. Restoration of miR-200a or the knockdown of SIRT1 prevented HSC activation and proliferation. We have established the SIRT1 transcript as subject to regulation by miR-200a, through miR-200a targeting of SIRT1 3'-UTR. Finally, HSC transfected with SIRT1-siRNA increased the levels of Notch1 protein and mRNA expression. CONCLUSIONS: Our study demonstrated that miR-200a regulates SIRT1/Notch1 expression during HSC activation and fibrosis.

MeCP2 silencing of LncRNA H19 controls hepatic stellate cell proliferation by targeting IGF1R.

Methyl-CpG-binding protein 2 (MeCP2) plays a key role in liver fibrosis. However, the potential mechanism of MeCP2 in liver fibrosis remains unclear. Early reports suggest that LncRNA H19 is important epigenetic regulator with critical roles in cell proliferation, but its role in hepatic fibrosis remains elusive. Sprague-Dawley rats liver fibrosis was generated by 12-weeks treatment with CCl4 intraperitoneal injection. HSC-T6 cells were used in vitro study. The expression levels of MeCP2, H19, IGF1R, α-SMA, and Col1A1 were estimated by Western blotting, qRT-PCR and Immunohistochemistry. HSC-T6 cells were transfected with MeCP2-siRNA, pEGF-C1-MeCP2, pEX-3-H19, and H19-siRNA. Finally, cell proliferation ability was assessed by the MTT assay. Here, we found that H19 was significantly down-regulated in HSCs and fibrosis tissues, and an opposite pattern is observed for MeCP2 and IGF1R. Silencing of MeCP2 blocked HSCs proliferation. Knockdown of MeCP2 elevated H19 expression in activated HSCs, and over-expression of MeCP2 inhibited H19 expression in activated HSCs. Moreover, we investigated the effect of H19 on IGF1R expression. Overexpression of H19 in HSCs repressed the expression of IGF1R, and an opposite pattern is observed for H19 silenced. In addition, we reported that overexpression of H19 inhibited the TGF-ß1-induced proliferation of HSCs. Furthermore, MeCP2 negative regulation of H19 by targeting the protein IGF1R. Taken together, these results demonstrated that MeCP2 silencing of H19 can alter the IGF1R overexpression, thus contributing to HSCs proliferation. These data could suggest the development of combination therapies that target the MeCP2.

Noncoding RNA as regulators of cardiac fibrosis: current insight and the road ahead.

Cardiac fibrosis is an important pathological feature of cardiac remodeling in heart diseases. The molecular mechanisms of cardiac fibrosis are unknown. Genomic analyses estimated that many noncoding DNA regions generate noncoding RNAs (ncRNAs). ncRNAs have emerged as key molecular players in the regulation of gene expression in different biological processes. Recent studies have started to reveal the importance of ncRNAs in heart development and suggest also an involvement in cardiac fibrosis. These molecules are emerging as important regulators of cellular process. Here, we review particularly focuses on the involvement of two large families of ncRNAs, namely microRNAs (miRNAs) and long noncoding RNAs (LncRNAs) in the regulation of cardiac fibrosis. Furthermore, we review the functions and role of ncRNAs in cardiac biology and discuss these reports and the therapeutic potential of ncRNAs for cardiac fibrosis associated with fibroblast activation and proliferation.

MeCP2 regulation of cardiac fibroblast proliferation and fibrosis by down-regulation of DUSP5.

Cardiac fibrosis is a complex pathological process that includes the abnormal proliferation of cardiac fibroblasts and deposition of the extracellular matrix (ECM) proteins and collagens. Methyl-CpG-binding protein 2 (MeCP2) is a multifunctional nuclear protein, and plays a key role in the fibrotic diseases. However, the potential role of MeCP2 in cardiac fibrosis remains unclear. We report that MeCP2 modulates cardiac fibrosis via down-regulation of dual-specificity phosphatase 5 (DUSP5), a nuclear phosphatase that negatively regulates prohypertrophic signaling by ERK1/2. MeCP2 is a critical participant in the epigenetic silencing of regulatory genes. Here, we found that down-regulation of DUSP5 in cardiac fibrosis is associated with MeCP2 over-expression. Treatment of cardiac fibroblasts with MeCP2-siRNA blocked proliferation. Knockdown of MeCP2 elevated DUSP5 expression in activated cardiac fibroblasts. Moreover, we investigated the effect of DUSP5 on the ERK1/2 activation. Our results demonstrated that MeCP2 modulates DUSP5 mediated activation of ERK1/2 in cardiac fibrosis. Taken together, these results indicated that MeCP2 acts as a key regulator of pathological cardiac fibrosis, promotes cardiac fibroblasts proliferation and fibrosis by down-regulation of DUSP5.

Emerging role of long noncoding RNAs in lung cancer: Current status and future prospects.

Lung cancer is the leading cause of cancer-related death worldwide with a 5-year survival rate of less than 15%, despite significant advances in both diagnostic and therapeutic approaches. Combined genomic and transcriptomic sequencing studies have identified numerous genetic driver mutations that are responsible for the development of lung cancer. Importantly, these approaches have also uncovered the widespread expression of "noncoding RNAs" including long noncoding RNAs (LncRNAs), which impact biologic responses through the regulation of mRNA transcription or translation. To date, most studies of the role of noncoding RNAs have focused on LncRNAs, which regulate mRNA translation via the RNA interference pathway. Although many of their attributes, such as patterns of expression, remain largely unknown, LncRNAs have key functions in transcriptional, post-transcriptional, and epigenetic gene regulation. Recent research showed that LncRNAs regulate flowering time in the lung cancer. In this review, we discuss these investigations into long noncoding RNAs were performed almost exclusively in lung cancer. Future work will need to extend these into lung cancer and to analyze how LncRNAs interact to regulate mRNA expression. From a clinical perspective, the targeting of LncRNAs as a novel therapeutic approach will require a deeper understanding of their function and mechanism of action.

Non-coding RNA-mediated epigenetic regulation of liver fibrosis.

Hepatic stellate cells (HSC) activation plays a key role in liver fibrosis. Numerous studies have indicated that non-coding RNAs (ncRNAs) control liver fibrosis and fibroblasts proliferation. Greater knowledge of the role of the ncRNAs-mediated epigenetic mechanism in liver fibrosis could improve understanding of the liver fibrosis pathogenesis. The aim of this review is to describe the present knowledge about the ncRNAs significantly participating in liver fibrosis and HSC activation, and look ahead on new perspectives of ncRNAs-mediated epigenetic mechanism research. Moreover, we will discuss examples of non-coding RNAs that interact with histone modification or DNA methylation to regulate gene expression in liver fibrosis. Diverse classes of ncRNAs, ranging from microRNAs (miRs) to long non-coding RNAs (LncRNAs), have emerged as key regulators of several important aspects of function, including cell proliferation, activation, etc. In addition, recent advances suggest the important role of ncRNAs transcripts in epigenetic gene regulation. Targeting the miRs and LncRNAs can be a promising direction in liver fibrosis treatment. We discuss new perspectives of miRs and LncRNAs in liver fibrosis and HSC activation, mainly including interaction with histone modification or DNA methylation to regulate gene expression. These epigenetic mechanisms form powerful ncRNAs surveillance systems that may represent new targets for liver fibrosis therapeutic intervention.