Silicon Nanowire Array Weaved by Carbon Chains for Stretchable Lithium-Ion Battery Anode.

To manufacture flexible batteries, it can be a challenge for silicon base anode materials to maintain structural integrity and electrical connectivity under bending and torsion conditions. In this work, 1D silicon nanowire array structures combined with flexible carbon chains consisting of short carbon nanofibers (CNFs) and long carbon nanotubes (CNTs) are proposed. The CNFs and CNTs serve as chain joints and separate chain units, respectively, weaving the well-ordered Si nanowire array into a robust and integrated configuration. The prepared flexible and stretchable silicon array anode exhibits excellent electrochemical performance during dynamic operation. A high initial specific capacity of 2856 mAh g-1 is achieved. After 1000 cycles, a capacity retention of 60% (1602 mAh g-1) is maintained. Additionally, the capacity attenuation is less than 1% after 100 bending cycles. This excellent cycling stability is obtained with a high Si loading of 6.92 mg cm-2. This novel approach offers great promise for the development of high-loading flexible energy-storage devices.

Circular RNA circCSPP1 knockdown attenuates doxorubicin resistance and suppresses tumor progression of colorectal cancer via miR-944/FZD7 axis.

BACKGROUND: Circular RNAs (circRNAs) have been reported to play vital roles in colorectal cancer (CRC). However, only a few circRNAs have been experimentally validated and functionally described. In this research, we aimed to reveal the functional mechanism of circCSPP1 in CRC. METHODS: 36 DOX sensitive and 36 resistant CRC cases participated in this study. The expression of circCSPP1, miR-944 and FZD7 were detected by quantitative real time polymerase chain reaction (qRT-PCR) and the protein levels of FZD7, MRP1, P-gp and LRP were detected by western blot. Cell proliferation, migration, invasion, and apoptosis were assessed by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) assay, transwell assay, or flow cytometry analysis, respectively. The interaction between miR-944 and circCSPP1 or frizzled-7 (FZD7) was predicted by Starbase 3.0 and verified by the dual luciferase reporter assay, RNA immunoprecipitation (RIP) assay and RNA pull down assay. Xenograft tumor assay was performed to examine the effect of circCSPP1 on tumor growth in vivo. RESULTS: The expression of circCSPP1 and FZD7 was upregulated while miR-944 expression was downregulated in doxorubicin (DOX)-resistant CRC tissues and cells. CircCSPP1 knockdown significantly downregulated enhanced doxorubicin sensitivity, suppressed proliferation, migration, invasion, and induced apoptosis in DOX-resistant CRC cells. Interestingly, we found that circCSPP1 directly downregulated miR-944 expression and miR-944 decreased FZD7 level through targeting to 3' untranslated region (UTR) of FZD7. Furthermore, circCSPP1 mediated DOX-resistant CRC cell progression and doxorubicin sensitivity by regulating miR-944/FZD7 axis. Besides, circCSPP1 downregulation dramatically repressed CRC tumor growth in vivo. CONCLUSION: Our data indicated that circCSPP1 knockdown inhibited DOX-resistant CRC cell growth and enhanced doxorubicin sensitivity by miR-944/FZD7 axis, providing a potential target for CRC therapy.

Use Chou's 5-steps rule to study how Baicalin suppresses the malignant phenotypes and induces the apoptosis of colorectal cancer cells.

Baicalin is a traditional Chinese herb purified from the root of Scutellaria baicalensis Georgi. In this study, we further analyzed the molecular mechanism behind the anti-tumor activity of Baicalin in colorectal cancer (CRC). The establishment of circular RNA (circRNA)/microRNA (miRNA)/messenger RNA (mRNA) axis was predicted by bioinformatic databases and verified by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Baicalin dose-dependently reduced the expression of circRNA myosin heavy chain 9 (circMYH9) in CRC cells. Baicalin exposure suppressed the malignant phenotypes of CRC cells, which were largely reversed by the overexpression of circMYH9. CircMYH9 functioned as a molecular sponge for miR-761. CircMYH9 overexpression protected CRC cells from Baicalin-induced injury partly through down-regulating miR-761. MiR-761 interacted with the 3' untranslated region (3' UTR) of hepatoma-derived growth factor (HDGF) mRNA. CircMYH9 up-regulated HDGF expression partly through sponging miR-761 in CRC cells. MiR-761 silencing counteracted the anti-tumor activity of Baicalin partly through up-regulating HDGF in CRC cells. Baicalin suppresses xenograft tumor growth in vivo, and this suppressive effect was partly reversed by the overexpression of circMYH9. In conclusion, Baicalin exhibited an anti-tumor activity in CRC cells partly through down-regulating circMYH9 and HDGF and up-regulating miR-761.

Solid-State Lithium Batteries with Ultrastable Cyclability: An Internal-External Modification Strategy.

A commonly used strategy to tackle the unstable interfacial problem between Li1.3Al0.3Ti1.7(PO4)3 (LATP) and lithium (Li) is to introduce an interlayer. However, this strategy has a limited effect on stabilizing LATP during long-term cycling or under high current density, which is due in part to the negative impact of its internal defects (e.g., gaps between grains (GBs)) that are usually neglected. Here, control experiments and theoretical calculations show clearly that the GBs of LATP have higher electronic conductivity, which significantly accelerates its side reactions with Li. Thus, a simple LiCl solution immersion method is demonstrated to modify the GBs and their electronic states, thereby stabilizing LATP. In addition to LiCl filling, composite solid polymer electrolyte (CSPE) interlayering is concurrently introduced at the Li/LATP interface to realize the internal-external dual modifications for LATP. As a result, electron leakage in LATP can be strictly inhibited from its interior (by LiCl) and exterior (by CSPE), and such dual modifications can well protect the Li/LATP interface from side reactions and Li dendrite penetration. Notably, thus-modified Li symmetrical cells can achieve ultrastable cycling for more than 3500 h at 0.4 mA cm-2 and 1500 h at 0.6 mA cm-2, among the best cycling performance to date.

Long noncoding RNA TUG1 regulates the progression of colorectal cancer through miR-542-3p/TRIB2 axis and Wnt/ß-catenin pathway.

BACKGROUND: Colorectal cancer (CRC) is one of the third normal malignancy worldwide. Taurine-upregulated gene 1 (TUG1), a member of long noncoding RNAs (lncRNAs), has been reported to be involved in various cancers. However, the mechanism underlying TUG1 in the progression of CRC remains unclear. METHODS: The expression of TUG1, microRNA-542-3p (miR-542-3p), and tribbles homolog 2 (TRIB2) in CRC tissues and cells (LoVo and HCT116) were detected by quantitative real-time PCR (qRT-PCR). Methyl thiazolyl tetrazolium (MTT), transwell and flow cytometry assays were employed to evaluate the effects of TUG1 in CRC cells. The interaction between miR-542-3p and TUG1 or TRIB2 were verified by dual-luciferase reporter assay. A xenograft tumor model in nude mice was established to investigate the biological role of TUG1 in CRC in vivo. RESULTS: TUG1 was increased in CRC tissues and cells (LoVo and HCT116) in contrast with adjacent normal tissues and normal intestinal mucous cells (CCC-HIE-2). Downregulation of TUG1 or TRIB2 suppressed the proliferation, migration, invasion, and induced apoptosis in CRC cells. And knockdown of TUG1 repressed tumor growth in vivo. Besides, overexpression of TRIB2 reversed the effects of TUG1 depletion on the progression of CRC. Meanwhile, TUG1 interacted with miR-542-3p and TRIB2 was a target of miR-542-3p. Furthermore, miR-542-3p knockdown or TRIB2 overexpression partly reversed the suppression effect of TUG1 depletion on the Wnt/ß-catenin pathway. CONCLUSIONS: TUG1 served as a tumor promoter, impeded the progression of CRC by miR-542-3p/TRIB2 axis to inactivate of Wnt/ß-catenin pathway, which providing a novel target for CRC treatment.