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19. ESCCAL-1 promotes cell-cycle progression by interacting with and stabilizing galectin-1 in esophageal squamous cell carcinoma.

Author

Cui, Yuanbo, Yan, Ming, Wu, Wei, Lv, Pengju, Wang, Jinwu, Huo, Yanping, Lou, Yanan, Ma, Xiwen, Chang, Jing, Guan, Fangxia, and Cao, Wei

Abstract

Long non-coding RNAs (LncRNAs) play important roles in the development of human esophageal squamous cell carcinoma (ESCC). Our previous studies have shown that knockdown of LncRNA ESCCAL-1 expression inhibits the growth of ESCC cells, but the mechanisms remain largely unknown. In this study, we show that over-expression of ESCCAL-1 promotes ESCC cell proliferation and cell-cycle progression by blocking ubiquitin-mediated degradation of an oncoprotein galectin-1 (Gal-1). Multiple LncRNA expression datasets as well as our own data together reveal that ESCCAL-1 is evidently up-regulated in ESCC tissues and exhibits promising diagnostic value. Over-expression of ESCCAL-1 augmented ESCC cell proliferation and cell-cycle progression, whereas down-regulation of ESCCAL-1 resulted in the opposite effects. Mechanistically, LncRNA ESCCAL-1 directly binds to Gal-1 and positively regulates its protein level without affecting its mRNA level. Up-regulation of Gal-1 facilitated ESCC cell proliferation and cell-cycle progress. Knockdown of Gal-1 mitigated the effects of ESCCAL-1-mediated high cellular proliferation, NF-κB signaling activation and tumorigenicity of ESCC cells. Thus, our findings provide novel insight into the mechanism by which ESCCAL-1 facilitates ESCC tumorigenesis and cell-cycle progression by interacting with and stabilizing Gal-1 protein, suggesting a potential therapeutic target for ESCC.

Published
2022

40. Molecular interaction regulation by adding a third component with high miscibility suppresses the energetic disorder and reduces energy loss for efficient ternary solar cells.

Author

Lin, Ruiying, Peng, Shichu, Luo, Zhenyu, Wu, Jiaxin, Jin, Yaocheng, Huo, Yanping, Xiao, Liangang, and Min, Yonggang

Abstract

In the advancement of organic solar cells (OSCs), the ternary strategy has emerged as an effective approach for fabricating devices with high photovoltaic performance. In this contribution, we have introduced a novel wide bandgap donor, PBTz-Cl, into the D18:L8-BO binary system to address the excessive aggregation of D18. PBTz-Cl exhibits excellent miscibility with D18 in ternary films due to their similar building blocks. Our findings show that the addition of PBTz-Cl forms a molecular alloy within the amorphous regions of D18. This not only boosts additional exciton generation in D18 through Förster resonance energy transfer, but also suppresses the non-radiative recombination energy loss (ΔE3) due to the reduced crystallinity difference between D18 and L8-BO by enhancing the crystallinity of L8-BO. The optimized ternary blend film exhibits superior microstructure morphology and enhanced charge dynamics, leading to enhanced photovoltaic performance and remarkable stability. The resulting OSCs show a remarkable increase in performance with a JSC of 25.30 mA cm−2, a VOC of 0.911 V, and an FF of 78.33%. Our study highlights the effectiveness of the strategy, which derives from the synergistic effects of compatible polymer donors to precisely regulate molecular packing and optimize film morphology for improved photovoltaic performance. [ABSTRACT FROM AUTHOR]

Published
2025
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41. In‐Situ Polymerized Solid/Quasi‐Solid Polymer Electrolyte for Lithium‐Metal Batteries: Recent Progress and Perspectives.

Author

Zhang, Hangyu, Xu, Xijun, Fan, Weizhen, Zhao, Jingwei, and Huo, Yanping

Subjects
POLYELECTROLYTES, SOLID electrolytes, ADDITION polymerization, ENERGY density, IONIC conductivity, SUPERIONIC conductors
Abstract

In pursuit of high energy density, lithium metal batteries (LMBs) are undoubtedly the best choice. However, leakage and inevitable dendrite growth in liquid electrolytes seriously hinder its practical application. Solid/quasi‐solid state electrolytes have emerged as an answer to solve the above issues. Especially, polymer electrolytes with excellent interface compatibility, high flexibility, and ease of machining have become a research hotspot for LMBs. Nevertheless, the interface contact between polymer electrolyte and inorganic electrode materials and the low ionic conductivity restrict its development. On account of these, in situ polymerized polymer electrolyte is proposed. Polymer solid electrolytes produced through in situ polymerization promote robust interface contact between the electrolyte and electrode while simplifying the preparation steps. This review summarized the latest research progress in in situ polymerized solid electrolytes for LMBs. These electrolytes were divided into three parts according to their polymerization methods: thermally induced polymerization, chemical initiator polymerization, ionizing radiation polymerization, and so on. Furthermore, we concluded the major challenges and future trends of in situ polymerized solid electrolytes for LMBs. It's hoped that this review will provide meaningful guidance on designing high‐performance polymer solid electrolytes for LMBs. [ABSTRACT FROM AUTHOR]

Published
2024
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43. ERα Coregulator TRIM28 Promotes Breast Cancer Progression by Activating the AKT/GSK3β Pathway.

Author

Fu, Linlin, Ma, Baodong, Zhang, Lan, Xu, Huikang, Chen, Wei, Wu, Di, Gao, Feng, and Huo, Yanping

Subjects
ESTROGEN receptors, BREAST cancer, CANCER invasiveness, CELL proliferation, CELL lines
Abstract

Estrogen receptor α (ERα) promotes the growth and survival of ER‐positive breast cancer (BC) cells. ER regulates ER expression target genes by directly binding to specific estrogen response elements, upon activation by estrogens. In this study, 106 proteins interacting with endogenous chromatin‐bound ER in a BC cell line MCF7 were identified using the RIME method. The interactome data showed that the tripartite motif containing 28 (TRIM28) is the most significantly enriched ER‐associated protein. This study provides evidence that TRIM28 expression improves ER transcriptional activity and promotes the BC cells proliferation, migration, and invasion of BC cells. The high expression of TRIM28 is associated with poor clinical outcomes in patients with ER‐positive BC. Mechanistic experiments indicate that TRIM28 expression activates the AKT/GSK3β pathway. To conclude, TRIM28 acts as a regulatory protein of ER and AKT signaling; therefore, it can be a target for the therapeutic interventions of BC. [ABSTRACT FROM AUTHOR]

Published
2024
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