The complete chloroplast genome of Salix lindleyana (salicaceae), a plateau plant species.

Salix lindleyana Wallich ex Andersson 1851 is a species of genus Salix which mainly grows on mountains above 3000 m at sea level in Qinghai-Tibetan Plateau (including the Himalayas and Hengduan Mountains). To determine its phylogenetic position within Salix, we reconstructed S. lindleyana complete chloroplast (cp) genome sequence by de novo assembly using whole-genome sequencing data. The completed chloroplast genome was 155,304 bp, with a total GC content of 36.7%. It had a very typical tetrad structure, including a large single-copy (LSC) region of 84,539 bp, a small single-copy (SSC) region of 16,161 bp, and two inverted repeats (IR) regions of 27,302 bp. A total of 132 functional genes were distributed in the chloroplast genome, including 87 protein-coding genes, 37 tRNA genes, and 8 rRNA genes. Phylogenetic analysis showed that S. lindleyana was clustered with Salix dasyclados Wimmer 1849 and Salix variegata Franchet 1887. The complete chloroplast genome of S. lindleyana provides potential genetic resources for further phylogenetic studies.

Non-synonymous substitution of evolutionarily conserved residue in Tau class glutathione transferases alters structural and catalytic features.

Plant-specific tau glutathione transferases (GSTs) are basically involved in catalysing γ-glutathione (GSH)-dependent conjugation reactions with pesticides and herbicides, which play an important role in the detoxification of pollutants. Given the lack of systematic biochemical and structural information on tau GSTs, the study of their mediated defence mechanisms against toxic compounds has been greatly hindered. Here, we reveal the importance of the Ile residue closely interacting with GSH for the structural stability and catalytic function of GST. Evolutionary conservation analysis indicated that the crucial G-site Ile55 in the SbGSTU6 was converted to Thr53 of SbGSTU7. The comparative biochemical data on SbGSTU6, SbGSTU7 and their mutants showed that the substitution of Ile by Thr caused significant decrease in the affinity and catalytic efficiency of the GSTs. The unfavourable structural flexibility and pKa distribution of the active cavity residues were also demonstrated. Crystallography studies and molecular dynamics simulations showed that the conversion resulted in the hydrogen bond recombination with GSH and conformational rearrangement of GST active cavity, in which the Ile residue was more conducive to the formation of enzyme substrate complexes. The extensive biochemical and structural data not only reveal the critical role of the conserved G-site Ile residue in catalysing GSH-conjugate reactions but also provide valuable resources for the development of GST engineering in analytical and agricultural biotechnology.

Self-Powered and Broadband Lead-Free Inorganic Perovskite Photodetector with High Stability.

Metal halide perovskite materials have opened up a great opportunity for high-performance optoelectronic devices owing to their extraordinary optoelectronic properties. More than lead halide ones, stable and nontoxic bismuth halide perovskites exhibit more promise in their future commercialization. In this work, we developed for the first time photodetectors based on full-inorganic Cs3Bi2I9-xBrx perovskites and modulate their performance by varying x in the composition systematically. Among those self-powered photodetectors, those based on Cs3Bi2I6Br3 shows the best performance with excellent photosensitivity of 4.1 × 104 at zero bias as well as the responsivity and detectivity reaching 15 mA/W and 4.6 × 1011 Jones, respectively. More strikingly, the full-inorganic perovskite photodetectors exhibit excellent stability in the ambient environment and can maintain over 96% of the initial value after 100 days owing to the high stability of the core perovskite film. The paper definitely paves an alternative and promising strategy for the design of future commercial photodetectors that are self-powered, stable, nontoxic, etc.

Knockdown of LINC00662 represses AK4 and attenuates radioresistance of oral squamous cell carcinoma.

BACKGROUND: LncRNAs play crucial roles in the development of carcinomas. However, the investigation of LINC00662 in Oral squamous cell carcinoma (OSCC) is still elusive. METHODS: qRT-PCR assay tested the expression levels of LINC00662, hnRNPC and AK4. With exposure to irradiation, CCK-8, colony formation, flow cytometry and western blot experiments, respectively determined the function of LINC00662 in the radiosensitivity of OSCC cells. Then RIP and western blot assays affirmed the interaction between hnRNPC protein and LINC00662 or AK4. Finally, rescue assays validated the regulation mechanism of LINC00662 in the radioresistance of OSCC. RESULTS: In the present report, LINC00662 was overexpressed in OSCC and its silencing could alleviate radioresistance of OSCC. Furthermore, the interaction between hnRNPC protein and LINC00662 or AK4 was uncovered. Besides, LINC00662 regulated AK4 mRNA stability through binding to hnRNPC protein. To sum up, LINC00662 modulated the radiosensitivity of OSCC cells via hnRNPC-modulated AK4. CONCLUSION: The molecular mechanism of the LINC00662/hnRNPC/AK4 axis was elucidated in OSCC, which exhibited a promising therapeutic direction for patients with OSCC.

Eukaryotic initiation Factor 4AIII facilitates hepatocellular carcinoma cell proliferation, migration, and epithelial-mesenchymal transition process via antagonistically binding to WD repeat domain 66 with miRNA-2113.

Hepatocellular carcinoma (HCC) is one of the malignant cancers with high incidence and mortality rates worldwide. RNA-binding protein eukaryotic initiation Factor 4A-III (eIF4AIII) is a carcinogene in the biological process of tumors and microRNA (miRNA)-2113 has rarely been studied in cancers, not to mention in HCC. The regulation mechanism between eIF4AIII and miR-2113 involved in HCC is yet to be explored. The purpose of this research is to probe the function role and associated underlying mechanism of eIF4AIII participated in HCC. The results revealed that eIF4AIII was overexpressed in HCC. Lost-of-function assays found that eIF4AIII knockdown, WD (Trp-Asp [tryptophan and asparaginic acid]) repeat domain 66 (WDR66) silence or miR-2113 promotion repressed cell proliferation, migration, and epithelial-mesenchymal transition (EMT) process in HCC. Furthermore, eIF4AIII could interact with WDR66 and further stabilize WDR66 messenger RNA. In addition, WDR66 was a target gene of miR-2113. Besides, WDR66 was antagonistically regulated by eIF4AIII and miR-2113. Rescue assays verified that eIF4AIII promoted HCC cell proliferation, migration, and EMT process via antagonistically binding to WDR66 with miR-2113. Taken together, these findings indicated an important role and a novel mechanism of eIF4AIII in HCC, providing an optional therapy for HCC patients.

Long non-coding RNA HCG11 modulates glioma progression through cooperating with miR-496/CPEB3 axis.

OBJECTIVES: It has been widely reported that long non-coding RNAs (lncRNAs) can participate in multiple biological processes of human cancers. lncRNA HLA complex group 11 (HCG11) has been reported in human cancers as a tumour suppressor. This study focused on investigating the function and mechanism of HCG11 in glioma. MATERIALS AND METHODS: Based on The Cancer Genome Atlas (TCGA) data set and qRT-PCR analysis, the expression pattern of HCG11 was identified in glioma samples. The mechanism associated with HCG11 downregulation was determined by mechanism experiments. Gain-of-function assays were conducted for the identification of HCG11 function in glioma progression. Mechanism investigation based on the luciferase reporter assay, RIP assay and pull-down assay was used to explore the downstream molecular mechanism of HCG11. The role of molecular pathway in the progression of glioma was analysed in accordance with the rescue assays. RESULTS: HCG11 was expressed at low level in glioma samples compared with normal samples. FOXP1 could bind with HCG11 and transcriptionally inactivated HCG11. Overexpression of HCG11 efficiently suppressed cell proliferation, induced cell cycle arrest and promoted cell apoptosis. HCG11 was predominantly enriched in the cytoplasm of glioma cells and acted as a competing endogenous RNAs (ceRNAs) by sponging micro-496 to upregulate cytoplasmic polyadenylation element binding protein 3 (CPEB3). CEPB3 and miR-496 involved in HCG11-mediated glioma progression. CONCLUSIONS: HCG11 inhibited glioma progression by regulating miR-496/CPEB3 axis.

Knockdown of LINC00511 promotes radiosensitivity of thyroid carcinoma cells via suppressing JAK2/STAT3 signaling pathway.

Thyroid carcinoma is the most widespread malignancy in endocrine system with the increasing incidence. Despite of the advanced approaches to the management of thyroid carcinoma, the therapeutic effects remain unpleasant largely due to the radiosensitivity of thyroid carcinoma cells. LncRNAs play important part in the tumorigenesis and development, especially in the radiosensitivity of tumor cells. However, their roles in thyroid carcinoma still needed to be explored deeply. The purpose of our research is to inspect the possible biological role and regulation mechanism of LINC00511 desirable for therapies of thyroid carcinoma patients. In the present study, LINC00511 was significantly overexpressed in thyroid carcinoma and its silencing boosted radiosensitivity of thyroid carcinoma cells. Then we unveiled that LINC00511 regulated JAK2/STAT3 signaling pathway which was resistant to radiation treatment. Besides, TAF1 modulated JAK2 at transcriptional level. Moreover, LINC00511 bound to TAF1 and further promoted JAK2 expression. In conclusion, rescue experiments verified that the radiosensitivity of thyroid carcinoma cells was attributed to LINC00511/TAF1/JAK2/STAT3 axis. The current paper investigated the underlying mechanism of LINC00511 and set a new therapeutic direction for the therapy of thyroid carcinoma.

Knockdown of lncRNA LEF1-AS1 inhibited the progression of oral squamous cell carcinoma (OSCC) via Hippo signaling pathway.

It is verified that long non-coding RNAs (lncRNAs) play crucial roles in various cancers. LncRNA LEF1-AS1 is a reported oncogene in colorectal cancer and glioblastoma. In this study, we unveiled that LEF1-AS1 markedly increased in oral squamous cell carcinoma (OSCC) tissues and cell lines. Besides, OSCC patients with high levels of LEF1-AS1 were apt to poor prognosis. Functionally, LEF1-AS1 knockdown inhibited cell survival, proliferation and migration, whereas enhanced cell apoptosis and induced G0/G1 cell cycle arrest in vitro. Consistently, LEF1-AS1 silence hindered tumor growth in vivo. Moreover, LEF1-AS1 inhibition stimulated the activation of Hippo signaling pathway through directly interacting with LATS1. Furtherly, we disclosed that LEF1-AS1 silence abolished the interaction of LEF1-AS1 with LATS1 while enhanced the binding of LATS1 to MOB, therefore promoting YAP phosphorylation but impairing YAP1 nuclear translocation. Additionally, we demonstrated that LEF1-AS1 regulated YAP1 translocation via a LATS1-dependent manner. Furthermore, we also uncovered that YAP1 overexpression abolished the suppressive impact of LEF1-AS1 repression on the biological processes of OSCC cells. In a word, we concluded that LEF1-AS1 served an oncogenic part in OSCC through suppressing Hippo signaling pathway by interacting with LATS1, suggesting the therapeutic and prognostic potential of LEF1-AS1 in OSCC.

Ultrafast unidirectional chiral rotation in the Z-E photoisomerization of two azoheteroarene photoswitches.

Unidirectional rotation represents a very important functional feature in photochemistry, such as in the design of light-driven molecular rotary motors. Great attention has recently been devoted to the unidirectional preference of the torsional motion of azobenzene and other molecules. Azoheteroarenes offer functional advantages over their more conventional azobenzene counterparts due to the introduction of heteroaromatic rings. In this paper, the Z-E photoisomerization dynamics of two azoheteroarenes, 1,2-bis(1-methyl-1H-imidazol-2-yl)diazene and 1,2-bis(1H-imidazol-2-yl)diazene, are investigated with trajectory surface-hopping molecular dynamics at the semi-empirical OM2/MRCI level. Starting from the S1 excited state of the M-helical Z-isomer of both azoheteroarenes, more than 99% of the trajectories decay to their ground states through the M-helical conical intersections by twisting about the central N[double bond, length as m-dash]N double bond. This chiral path preference can be well understood by the energy profiles generated by the linear interpolation between the Franck-Condon geometry of the M-helical Z-isomer and the relevant S1/S0 conical intersections. The Z-E photoisomerization mechanisms of these two azoheteroarenes display a higher preference for unidirectional rotary dynamics under a chiral path than their counterpart azobenzene.

LncRNA PRNCR1 interacts with HEY2 to abolish miR-448-mediated growth inhibition in non-small cell lung cancer.

It has been announced in accumulative studies that non-coding (nc)RNAs are responsible for a varieties of biological behaviors during the progression of tumors. As two subgroups of ncRNAs family, micro (mi)RNAs can interact with long non-coding (lnc)RNAs, thereby forming ceRNA network. In this study, miR-448 was expressed higher in NSCLC tissues (P < 0.01) and NSCLC cell lines (P < 0.01). Moreover, low expression of miR-448 predicted poor prognosis for patients with NSCLC (P < 0.001). Functional assays revealed the anti-oncogenic function of miR-448 in NSCLC by inhibiting cell proliferation, invasion, migration and epithelial-mesenchymal transition (EMT). Mechanically, miR-448 was found to be negatively regulated by lncRNA PRNCR1 (prostate cancer non-coding RNA 1). Moreover, HEY2 (Hairy and enhancer of split-related with YRPW motif protein 2) was demonstrated to be the target mRNA of miR-448 in NSCLC cells. All mechanism experiments revealed that lncRNA PRNCR1 exerted ceRNA function in NSCLC by regulating miR-448 and HEY2. To validate the function of PRNCR1-miR-488-HEY2 network in NSCLC progression, rescue assays were conducted. Taken all together, we confirmed that lncRNA PRNCR1 upregulates HEY2 to promote tumor progression in NSCLC by competitively binding miR-448.