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Papillary thyroid carcinoma (PTC) is a common malignancy worldwide. LncRNA LINC00704 (mitotically associated long non-coding RNA) was reported as a crucial regulator in PTC. However, the biological mechanism of LINC00704 action remains unclear in PTC. The mRNA levels of LINC00704, miR-204-5p, and high-mobility group box 1 (HMGB1) were measured by quantitative reverse transcription-polymerase chain reaction (qRT-PCR) assay. HMGB1, proliferating cell nuclear antigen (PCNA), and cyclin D1 protein levels were detected using the Western blot assay. The binding relationship between miR-204-5p and LINC00704 or HMGB1 was predicted by LncBase Predicted v.2 or TargetScan, respectively, and then validated by dual luciferase reporter assay. Cell viability, cell cycle, cell migration and invasion, and migration ratio were assessed by MTT, flow cytometry, transwell cell migration and invasion, and wound-healing assays, respectively. Results suggested that LINC00704 and HMGB1 were elevated and miR-204-5p decreased in PTC tissues and cells. Furthermore, rescue experiments demonstrated that the miR-204-5p inhibitor alleviated the inhibitory effects of LINC00704 knockdown on cell proliferation, cell cycle, migration, and invasion. Meanwhile, miR-204-5p overexpression repressed proliferation, migration, and invasion by targeting HMGB1. Mechanical analysis discovered that LINC00704 could act as an miR-204-5p sponge to modulate HMGB1 expression. In conclusion, LINC00704 promoted PTC cell proliferation, cell cycle, migration, and invasion by the miR-204-5p/HMGB1 axis, providing a novel therapeutic target for PTC patients.

Byline: Duan. Xiao, Yihui. Lin, Xiaofeng. Wang, Canhong. Yang, Xiaoyu. Huang, Bo. Fu, Qingzhu. Wei, Tianming. Lü Sir, Anti-N-methyl D-aspartate receptor (NMDAR) encephalitis is a novel NMDAR-mediated form of autoimmune [...]

N6‐methyladenosine (m6A) and long noncoding RNAs (lncRNAs) are both crucial regulators in non‐small‐cell lung cancer (NSCLC) tumorigenesis. However, the pathological roles of m6A and lncRNAs in NSCLC progression are still limited and undefined. Here, lncRNA ABHD11‐AS1 was upregulated in NSCLC tissue specimens and cells and the ectopic overexpression was closely correlated with unfavorable prognosis of NSCLC patients. Functionally, ABHD11‐AS1 promoted the proliferation and Warburg effect of NSCLC. Mechanistically, m6A profile was analyzed by methylated RNA immunoprecipitation sequencing (MeRIP‐Seq). MeRIP‐Seq presented that there was m6A modification site in ABHD11‐AS1. m6A methyltransferase‐like 3 (METTL3) installed the m6A modification and enhanced ABHD11‐AS1 transcript stability to increase its expression. In conclusion, our findings highlight the function and mechanism of METTL3‐induced ABHD11‐AS1 in NSCLC and inspire the understanding of m6A and lncRNA in cancer biology. [ABSTRACT FROM AUTHOR]

Multivariate analysis within central composite design is applied to simplify an optimization procedure and explore the interactions among experimental parameters in analytical chemistry. In this study, central composite design was used to identify the optimal capillary electrophoresis conditions with electroosmotic flow modulation to determine seven exfoliating agents in cosmetics. The influence of phosphate concentration, cetyltrimethylammonium bromide concentration, and methanol percentage on the response was evaluated by the use of the chromatographic exponential function to simultaneously investigate the resolution and separation under sixteen sets of capillary electrophoresis conditions. The optimized conditions were 150 mM phosphate solution (pH = 7) containing 0.5 mM cetyltrimethylammonium bromide, 3 mM γ-cyclodextrin, and 25% methanol as the running buffer. To shorten the analysis time, an electroosmotic flow modulating agent (cetyltrimethylammonium bromide) was added to the separation buffer. Calibration plots were linear (r ≧ 0.998) with high precision and accuracy in the homemade cosmetic matrix. The exfoliating agents in two commercial cosmetic products were determined using the optimized conditions, and the results correlated well with results obtained by high-performance liquid chromatography–mass spectrometry. [ABSTRACT FROM AUTHOR]

Using laser 40Ar/39Ar dating method, we have gotten the metamorphic ages of lawsonite blueschist and epidote blueschist from Jiuquan, northern Qilian Mountain, NW China. The high quality laser 40Ar/39Ar dating of glaucophane from lawsonite blueschist gives an isochron age of 413±5 Ma. The isochron age obtained from phengite in epidote blueschist is 415±7 Ma. These data, combining with peak metamorphic P-T conditions and regional geological setting, allow us to infer that the lower limit of the ages of the prograde subduction metamorphism from lawsonite blueschist facies to epidote blueschist facies occurred at ca. 413--415 Ma, which also suggests that the formation of lawsonite blueschist in the northern Qilian Mountain maybe resulted from the corner flow in the cold subduction zone. This study shows that the final closing time of the northern Qilian remnant oceanic basin is about 413--415 Ma, which also represents the convergent age between the North China Craton and the Qaidam block. [ABSTRACT FROM AUTHOR]

N 6 -methyladenosine (m 6 A) and long noncoding RNAs (lncRNAs) are both crucial regulators in non-small-cell lung cancer (NSCLC) tumorigenesis. However, the pathological roles of m 6 A and lncRNAs in NSCLC progression are still limited and undefined. Here, lncRNA ABHD11-AS1 was upregulated in NSCLC tissue specimens and cells and the ectopic overexpression was closely correlated with unfavorable prognosis of NSCLC patients. Functionally, ABHD11-AS1 promoted the proliferation and Warburg effect of NSCLC. Mechanistically, m 6 A profile was analyzed by methylated RNA immunoprecipitation sequencing (MeRIP-Seq). MeRIP-Seq presented that there was m 6 A modification site in ABHD11-AS1. m 6 A methyltransferase-like 3 (METTL3) installed the m 6 A modification and enhanced ABHD11-AS1 transcript stability to increase its expression. In conclusion, our findings highlight the function and mechanism of METTL3-induced ABHD11-AS1 in NSCLC and inspire the understanding of m 6 A and lncRNA in cancer biology., (© 2020 Wiley Periodicals LLC.)

Purpose: Gallbladder sarcomatoid carcinoma is a rare cancer with no clinical standard treatment. With the rapid development of next generation sequencing, it has been able to provide reasonable treatment options for patients based on genetic variations. However, most cancer drugs are not approval for gallbladder sarcomatoid carcinoma indications. The correlation between drug response and a genetic variation needs to be further elucidated., Experimental Design: Three patient-derived cells-JXQ-3D-001, JXQ-3D-002, and JXQ-3D-003, were derived from biopsy samples of one gallbladder sarcomatoid carcinoma patient with progression and have been characterized. In order to study the relationship between drug sensitivity and gene alteration, genetic mutations of three patient-derived cells were discovered by whole exome sequencing, and drug screening has been performed based on the gene alterations and related signaling pathways that are associated with drug targets., Results: It has been found that there are differences in biological characteristics such as morphology, cell proliferation, cell migration and colony formation activity among these three patient-derived cells although they are derived from the same patient. Their sensitivities to the chemotherapy drugs-Fluorouracil, Doxorubicin, and Cisplatin are distinct. Moreover, none of common chemotherapy drugs could inhibit the proliferations of all three patient-derived cells. Comprehensive analysis of their whole exome sequencing demonstrated that tumor-associated genes TP53, AKT2, FGFR3, FGF10, SDHA, and PI3KCA were mutated or amplified. Part of these alterations are actionable. By screening a set of compounds that are associated with the genetic alteration, it has been found that GDC-0941 and PF-04691502 for PI3K-AKT-mTOR pathway inhibitors could dramatically decrease the proliferation of three patient-derived cells. Importantly, expression of phosphorylated AKT and phosphorylated S6 were markedly decreased after treatments with PI3K-AKT-mTOR pathway inhibitors GDC-0941 (0.5 μM) and PF-04691502 (0.1 μM) in all three patient-derived cells. These data suggested that inhibition of the PI3K-AKT-mTOR pathway that was activated by PIK3CA amplification in all three patient-derived cells could reduce the cell proliferation., Conclusions: A patient-derived cell model combined with whole exome sequencing is a powerful tool to elucidate relationship between drug sensitivities and genetic alternations. In these gallbladder sarcomatoid carcinoma patient-derived cells, it is found that PIK3CA amplification could be used as a biomarker to indicate PI3K-AKT-mTOR pathway activation. Block of the pathway may benefit the gallbladder sarcomatoid carcinoma patient with this alternation in hypothesis. The real efficacy needs to be confirmed in vivo or in a clinical trial.