Dissolution and recrystallization of perovskite induced by N-methyl-2-pyrrolidone in a closed steam annealing method

High quality perovskite films with large columnar grains are greatly desired for efficient perovskite solar cells. Here, low volatility N-methyl-2-pyrrolidone(NMP) was added in MAI/IPA solution in a two-step spin-coating method, which promoted the conversion of lead iodide to perovskite. The perovskite films were annealed by a closed-steam annealing method to prolong the recrystallization process of perovskite films assisted by the residual NMP. It leaded to high quality CH_3NH_3PbI_3 perovskite films with large columnar grains due to its enhancement of the Oswald ripening. The large grain perovskite film leaded to efficient carrier transformation and injection, and low recombination. The photovoltaic performance of the perovskite solar cells was improved significantly.

RBM25 depletion suppresses the growth of colon cancer cells through regulating alternative splicing of MNK2

Increasing evidence suggests that deregulated RNA splicing factors play critical roles in tumorigenesis;however,their specific involvement in colon cancer remains largely unknown.Here we report that the splicing factor RBM25 is overexpressed in colon cancer,and this increased expression correlates with a poor prognosis of patients with colon cancer.Functionally,RBM25 ablation suppresses the growth of colon cancer cells both in vitro and in vivo.Mechanistically,our transcriptome-wide analysis of splicing events revealed that RBM25 regulates a large number of cancer-related alternative splicing events across the human genome in colon cancer.Particularly,RBM25 regulates the splicing of MNK2 by interacting with the poly G rich region in exon 14a,thereby inhibiting the selection of the proximal 3'splice site(ss),resulting in the production of the oncogenic short isoform,MNK2b.Knockdown of RBM25 leads to an increase in the MNK2a isoform and a decrease in the MNK2b isoform.Importantly,re-expression of MNK2b or blocking the 3′ss of the alternative exon 14a with ASO partially reverses the RBM25 knockdown mediated tumor suppression.Moreover,MNK2b levels were significantly increased in colon cancer tissues,which is positively correlated with the expression level of RBM25.Collectively,our findings uncover the critical role of RBM25 as a key splicing factor in colon cancer,suggesting its potential as a prognostic marker and therapeutic target.

RBM4 dictates ESCC cell fate switch from cellular senescence to glutamine-addiction survival through inhibiting LKB1-AMPK-axis

Cellular senescence provides a protective barrier against tumorigenesis in precancerous or normal tissues upon distinct stressors.However,the detailed mechanisms by which tumor cells evade premature senescence to malignant progression remain largely elusive.Here we reported that RBM4 adversely impacted cellular senescence to favor glutamine-dependent survival of esophageal squamous cell carcinoma(ESCC)cells by dictating the activity of LKB1,a critical governor of cancer metabolism.The level of RBM4 was specifically elevated in ESCC compared to normal tissues,and RBM4 overexpression promoted the malignant phenotype.RBM4 contributed to overcome H-RAS-or doxorubicin-induced senescence,while its depletion caused P27-dependent senescence and proliferation arrest by activating LKB1-AMPK-mTOR cascade.Mechanistically,RBM4 competitively bound LKB1 to disrupt the LKB1/STRAD/MO25 heterotrimeric complex,subsequently recruiting the E3 ligase TRIM26 to LKB1,promoting LKB1 ubiquitination and degradation in nucleus.Therefore,such molecular process leads to bypassing senescence and sustaining cell proliferation through the activation of glutamine metabolism.Clinically,the ESCC patients with high RBM4 and low LKB1 have significantly worse overall survival than those with low RBM4 and high LKB1.The RBM4 high/LKB1 low expression confers increased sensitivity of ESCC cells to glutaminase inhibitor CB-839,providing a novel insight into mechanisms underlying the glutamine-dependency to improve the efficacy of glutamine inhibitors in ESCC therapeutics.