Improved Carrier Management via a Multifunctional Modifier for High-Quality Low-Bandgap Sn-Pb Perovskites and Efficient All-Perovskite Tandem Solar Cells.

All-perovskite tandem solar cells (TSCs) hold great promise in terms of ultrahigh efficiency, low manufacturing cost, and flexibility, stepping forward to the next-generation photovoltaics. However, their further development is hampered by the relatively low performance of low-bandgap (LBG) tin (Sn)-lead (Pb) perovskite solar cells (PSCs). Improving the carrier management, including suppressing trap-assisted non-radiative recombination and promoting carrier transfer, is of great significance to enhance the performance of Sn-Pb PSCs. Herein, a carrier management strategy is reported for using cysteine hydrochloride (CysHCl) simultaneously as a bulky passivator and a surface anchoring agent for Sn-Pb perovskite. CysHCl processing effectively reduces trap density and suppresses non-radiative recombination, enabling the growth of high-quality Sn-Pb perovskite with greatly improved carrier diffusion length of >8 µm. Furthermore, the electron transfer at the perovskite/C60 interface is accelerated due to the formation of surface dipoles and favorable energy band bending. As a result, these advances enable the demonstration of champion efficiency of 22.15% for CysHCl-processed LBG Sn-Pb PSCs with remarkable enhancement in both open-circuit voltage and fill factor. When paired with a wide-bandgap (WBG) perovskite subcell, a certified 25.7%-efficient all-perovskite monolithic tandem device is further demonstrated.

Prognostic signature related to the immune environment of oral squamous cell carcinoma.

Oral squamous cell carcinoma (OSCC) prognosis remains poor. Here we aimed to identify an effective prognostic signature for predicting the survival of patients with OSCC. Gene-expression and clinical data were obtained from the Cancer Genome Atlas database. Immune microenvironment-associated genes were identified using bioinformatics. Subtype and risk-score analyses were performed for these genes. Kaplan-Meier analysis and immune cell infiltration level were explored in different subtypes and risk-score groups. The prognostic ability, independent prognosis, and clinical features of the risk score were assessed. Furthermore, immunotherapy response based on the risk score was explored. Finally, a conjoint analysis of the subtype and risk-score groups was performed to determine the best prognostic combination. We found 11 potential prognostic genes and constructed a risk-score model. The subtype cluster 2 and a high-risk group showed the worst overall survival; differences in survival status might be due to the different immune cell infiltration levels. The risk score showed good performance, independent prognostic value, and valuable clinical application. Higher risk scores showed higher Tumor Immune Dysfunction and Exclusion scores, indicating that patients with a high-risk score were less likely to benefit from immunotherapy. Finally, conjoint analysis for the subgroups and risk groups showed the best predictive ability.

LINC01123 is associated with prognosis of oral squamous cell carcinoma and involved in tumor progression by sponging miR-34a-5p.

OBJECTIVE: Oral squamous cell carcinoma (OSCC) is a malignant tumor. This study aimed to investigate the role of a long noncoding RNA (lncRNA), LINC01123, in OSCC prognosis and progression and to explore the underlying mechanisms. STUDY DESIGN: OSCC tissues were collected from 102 patients, and 4 OSCC cell lines were analyzed. The expression levels of LINC01123 and miR-34a-5p were estimated using quantitative real-time polymerase chain reaction (qRT-PCR). Cell counting kit-8 (CCK-8) and Transwell assays were used to assess the proliferation, migration, and invasion of OSCC cells. Kaplan-Meier survival analysis was used to analyze the prognostic value of LINC01123 in OSCC. RESULTS: The analysis results showed that LINC01123 was overexpressed in OSCC tumor tissues; also, the prognosis of patients with OSCC with high LINC01123 expression levels was poor. The knockdown of LINC01123 inhibited the proliferation, migration, and invasion of OCSS cells. MiR-34a-5p was a target of LINC01123, and its inhibitor could reverse the effect of silenced LINC01123 on the progression of OSCC. CONCLUSIONS: Highly expressed LINC01123 was associated with poor prognosis of OSCC and regulated OSCC cell proliferation, invasion, and migration by sponging miR-34a-5p. Therefore, the LINC01123/miR-34a-5p axis may provide new ideas for the prognosis and treatment of OSCC.

Active vitamin D activates chondrocyte autophagy to reduce osteoarthritis via mediating the AMPK-mTOR signaling pathway.

Osteoarthritis (OA) is a common joint degenerative disease. Vitamin D (VD) is essential for bone health. We hypothesized that active VD could be used as a therapeutic treatment for OA. Low serum levels of 25-hydroxyvitamin D [25(OH)D] have been found in patients with OA, and thus the serum level of VD could be diagnostic of OA. To test this, we established a mouse model of OA. The results from staining with hematoxylin-eosin and Safranin O - Fast Green indicated that active VD reduced the symptoms of OA in mice. The results from Western blotting indicated that treatment with VD increased the activity of the p-AMPK-AMPK signaling pathway and decreased the p-mTOR-mTOR pathway; it also increased the ratio of LC3II:LC3I antibodies and the protein expression levels of Beclin-1, but decreased the level of p62. Further, treatment with VD reduced the levels of tumor necrosis factor-α and interleukin-6 both in cartilage tissues and in chondrocytes. Administration of the AMPK inhibitor compound C and autophagy inhibitor 3-methyladenine (3-MA) reversed these changes following VD treatment. In addition, the results from transfection with mRFP-GFP-LC3 indicated that active VD led to autophagosome aggregation in OA chondrocytes. 3-MA inhibited cell autophagy and promoted inflammation in OA. This study provides evidence that active VD activate chondrocyte autophagy to reduce OA inflammation via activating the AMPK-mTOR signaling pathway. Treatment with active VD could be a novel therapeutic option for OA.

GPC5, a tumor suppressor, is regulated by miR-620 in lung adenocarcinoma.

In the current study, a proportion of lung adenocarcinoma was shown to reduce GPC5 expression in the absence of transcriptional silencing of the tumor suppressor gene, GPC5, by aberrant methylation of CpG islands. It was hypothesized that the loss of GPC5 expression is associated with upregulation of miR­620 in human lung adenocarcinoma tissue compared with the matched normal lung tissue. The downregulation of GPC5 in lung adenocarcinoma cell lines is regulated by miR­620 through binding of the 3'­untranslated region. Furthermore, blockage of miR­620 inhibited the proliferation, migration and invasion of lung adenocarcinoma cells by directly regulating GPC5, and GPC5 knockdown eliminates this phenotype. These results provided a novel insight into the mechanism of miRNA regulation in lung adenocarcinoma.

MicroRNA-25 regulates small cell lung cancer cell development and cell cycle through cyclin E2.

PURPOSE: We intended to examine the underlying mechanism of microRNA-25 (miR-25) in regulating small cell lung cancer (SCLC). METHODS: The miR-25 expression was measured by quantitative RT-PCR (qRT-PCR) in 5 SCLC cell lines and 9 human SCLC tissues. In SCLC cell line H510A cells, endogenous miR-25 was downregulated by stable transfection of antisense oligonucleotide of miR-25 (miR-25-as). Then the effects of miR-25 downregulation on SCLC growth, invasion and chemoresistance were assessed by MTT, migration and cisplatin assays, respectively. Furthermore, the effects of miR-25 downregulation on cancer cell cycle arrest, production of cell cycle proteins cyclin E2 and CDK2 were examined by cell cycle assay, western blot and luciferase assays, respectively. Finally, cyclin E2 was over-expressed in H510A cells to investigate its effect on miR-25 mediated SCLC regulation. RESULTS: In both SCLC cells and human SCLC tumor tissues, miR-25 was overexpressed. Down-regulation of miR-25 in H510A cells significantly reduced cancer cell growth, invasive capability and resistance to cisplatin. Also, it induced G1 cell cycle arrest and downregulated cell cycle related proteins cyclin E2 and CDK2. Luciferase assay demonstrated cyclin E2 was directly targeted by miR-25. Overexpression of cyclin E2 in H510A cells reversed the cell cycle arrest and restored invasive capability impaired by miR-25 downregulation. CONCLUSIONS: Our study shows miR-25 is overexpressed in SCLC and acting as oncogenic regulator by regulating cyclin E2.

TIAM2 enhances non-small cell lung cancer cell invasion and motility.

BACKGROUND: TIAM2, a Rac guanine nucleotide exchange factor, is closely associated with cell adherence and migration. Here, we aimed to investigate the role of TIAM2 in non-small cell lung cancer (NSCLC) cells. MATERIALS AND METHODS: A small interference RNA (siRNA) was introduced to silence the expression of TIAM2. Invasion and motility assays were then performed to assess the invasion and motility potential of NSCLC cells. GST-pull down assays were used to detect activation of Rac1. RESULTS: TIAM2 was highly expressed in NSCLC cells. Knockdown of TIAM2 inhibited the invasion and motility, and suppressed activation of Rac1. Further experiments demonstrated that knockdown of TIAM2 could up-regulate the expression of E-cadherin, and down- regulate the expression of MMP-3, Twist and Snail. CONCLUSIONS: Our data suggest that TIAM2 can promote invasion and motility of NSCLC cells. Activation of Rac1 and regulation of some EMT/invasion-related genes may be involved in the underlying processes.