Head and neck squamous carcinoma (HNSC) is the most prevalent malignancy of the head and neck regions. Long noncoding RNAs (lncRNAs) are vital in tumorigenesis regulation. However, the role of lncRNAs in HNSC requires further exploration. Herein, through bioinformatic assays using The Cancer Genome Atlas (TCGA) datasets, rapid amplification of cDNA ends (RACE) assays, and RNA-FISH, we revealed that a novel cytoplasmic transcript, HNSC-associated transcript 1 (HNSCAT1, previously recognized as linc01269), was downregulated in tumor samples and advanced tumor stages and was also associated with favorable outcomes in HNSC. Overexpression of HNSCAT1 triggered treatment efficacy in HNSCs both in vivo and in vitro. More importantly, through high-throughput transcriptome analysis (RNA-seq, in NODE database, OEZ007550), we identified KRT80, a tumor suppressor in HNSC, as the target of HNSCAT1. KRT80 expression was modulated by lncRNA HNSCAT1 and presented a positive correlation in tumor samples ( R = 0.52 , p < 0.001 ). Intriguingly, we identified that miR-1245 simultaneously interacts with KRT80 and HNSCAT1, which bridges the regulatory function between KRT80 and HNSCAT1. Conclusively, our study demonstrated that lncRNA HNSCAT1 functions as a necessary tumor inhibitor in HNSC, which provides a novel mechanism of lncRNA function and provides alternative targets for the diagnosis and treatment of HNSC.

Nowadays, the compound fine-blanking forming process is one of the most important processes to produce complicate multifunctional parts without subsequent machining. However, the big die-roll occurs in the sharp area is a common problem in this process. In this paper, the method with negative punch-die clearance was proposed to solve this problem by comparing three feasible plans. In addition, the influence on the process with different value of the negative punch-die clearance was studied by the finite element method (FEM). The results of this study verified that the process with suitable value of the negative punch-die clearance can result in significant decrease of the die-roll size. The relationship between the material flow near the region of die-roll and the punch-die clearance was also clarified.

Purpose: To externally validate the performance of the S-GRAS score and a model from the SEER database in a Chinese cohort of patients with adrenocortical carcinoma (ACC). Methods: We first developed a model using data from the SEER database, after which we retrospectively reviewed 51 ACC patients hospitalized between 2013 and 2018, and we finally validated the model and S-GRAS score in this Chinese cohort. Results: Patient age at diagnosis, tumor size, TNM stage, and radiotherapy were used to construct the model, and the Harrell’s C-index of the model in the training set was 0.725 (95%CI: 0.682-0.768). However, the 5-year AUC of the model in the validation cohort was 0.598 (95%CI: 0.487-0.708). The 5-year AUC of the ENSAT stage was 0.640 (95%CI: 0.543-0.737), but the Kaplan-Meier curves of stage I and II overlapped in the validation cohort. The resection status (P=0.066), age (P=0.68), Ki67 (P=0.69), and symptoms (P=0.66) did not have a significant impact on cancer-specific survival in the validation cohort. In contrast, the S-GRAS score group showed better discrimination (5-year AUC: 0.683, 95%CI: 0.602-0.764) than the SEER model or the ENSAT stage. Conclusion: The SEER model showed favorable discrimination and calibration ability in the training set, but it failed to distinguish patients with various prognoses in our institution. In contrast, the S-GRAS score could effectively stratify patients with different outcomes.

Background Keloid is a dermal fibroproliferative disease with various etiologies and unclear pathogenesis. Recent studies have revealed that circular RNAs (circRNAs) exerted regulatory functions through a competing endogenous RNA (ceRNA) pathway in keloid progression. However, the expression profiles of circRNAs in keloid dermal tissues (KDTs) remain unknown. This study aimed to identify differentially expressed circRNAs (DECs) and genes (DEGs) in KDTs, as well as to investigate the potential biological functionsof circRNAs based on the circRNA-miRNA-mRNA ceRNA network. Results Through high-throughput RNA sequencing (RNA-seq), we revealed 3467 DEGs (865 up- and 2602 down-regulated) and 330 DECs (162 up- and 168 down-regulated) in KDTs. To reveal the functions of DECs preliminarily, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were performed for the host genes. Further, the up- and down-regulated DECs-miRNAs-DEGs regulatory networks were constructed, respectively. The functional prediction for the target genes showed that the up-regulated ceRNA network was associated with extracellular matrix and multiple cellular functions. The down-regulated ceRNA network was enriched in cell-cell junction and other biological processes. Cytoscape was used to visualize each network's protein-protein interaction (PPI) network and identify hub genes. By quantitative Real-Time PCR (qRT-PCR), hsa_circ_0060927, hsa_circ_0071410, hsa_circ_0058092, hsa_circ_0002874, hsa_circ_0004682, hsa_circ_0072688, hsa_circ_0006401, and hsa_circ_0055954 were identified significantly up-regulated in KDTs. Within, hsa_circ_0072688, which was up-regulated both in KDTs and keloid dermal fibroblasts (KDFs), and located in the cytoplasm, might be a key circRNA and affect the progression of keloid by impacting extracellular matrix, cell adhesion, and cell apoptosis, etc. Conclusion This study not only filled a gap in the circRNA library of KDTs but also laid a foundation for probing the biological function of DECs in keloids. Hsa_circ_0072688 was thought to be a key circRNA and more experimental support is needed.

Background: Compensatory renal growth following nephrectomy is common. We try to explore the compensatory capacity of the living-related donor’s remnant kidney and recipient’s transplanted kidney in terms of the glomerular filtration rate (GFR) one month after transplantation. Methods: Clinical data of 94 patients who received living-related kidney transplantation in our hospital between June 2007 and December 2017 were reviewed retrospectively. GFR was calculated by 99mTc-DTPA detection. The GFR compensatory capacity of donor’s remnant and donated kidneys in their new milieus after transplantation was compared. The differential value (D-value) of split renal function was defined as postoperative GFR - preoperative ipsilateral GFR. The compensatory percentage (C-percentage) of split renal function was defined as (postoperative GFR - preoperative ipsilateral GFR)/preoperative ipsilateral GFR. Results: The median D-value of the donor’s remnant kidney increased by 20.8 ml/(min·1.73m2)[IQR=8.9-29.6 ml/(min·1.73m2)] with a C-percentage of 46.6% (IQR=17.0%-73.0%). The median D-value of the donated kidney increased by 30.6 ml/(min·1.73m2)[IQR=19.8-42.3 ml/(min·1.73m2)] with a C-percentage of 67.8% (IQR=39.6%-94.7%). Multivariable analysis showed that only split preoperative GFR in the donor was the independent predictor for C-percentage of the split kidney. Conclusions: Renal function could be well preserved and compensated after kidney donation in most donors and recipients in Chinese population. Healthy donors with a good GFR before operation possessed a mighty functional compensation capacity.

Background Impaired wound re-epithelialization contributes to cutaneous barrier reconstruction dysfunction. Recently, N6-methyladenosine (m6A) RNA modification has been shown to participate in the determination of RNA fate, and its aberration triggers the pathogenesis of numerous diseases. Howbeit, the function of m6A in wound re-epithelialization remains enigmatic. Methods Alkbh5‒/‒ mouse was constructed to study the rate of wound re-epithelialization after ALKBH5 ablation. Integrated high-throughput analysis combining methylated RNA immunoprecipitation sequencing (MeRIP-seq) and RNA-seq was used to identify the downstream target of ALKBH5. In vitro and in vivo rescue experiments were conducted to verify the role of the downstream target on the functional phenotype of ALKBH5-deficient cells or animals. Furthermore, the interacting reader protein and regulatory mechanisms were determined through RIP-qPCR, RNA pull–down, and RNA stability assays. Results ALKBH5 was specifically upregulated in the wound edge epidermis. Ablation of ALKBH5 suppressed keratinocyte migration and resulted in delayed wound re-epithelialization in Alkbh5‒/‒ mouse. Integrated high-throughput analysis revealed that PELI2, an E3 ubiquitin protein ligase, serves as the downstream target of ALKBH5. Concordantly, exogenous PELI2 supplementation partially rescued keratinocyte migration and accelerated re-epithelialization in ALKBH5-deficient cells, both in vitro and in vivo. In terms of its mechanism, ALKBH5 promoted PELI2 expression by removing the m6A modification from PELI2 mRNA and enhancing its stability in a YTHDF2-dependent manner. Conclusions This study identifies ALKBH5 as an endogenous accelerator of wound re-epithelialization, thereby benefiting the development of a reprogrammed m6A targeted therapy for refractory wounds. Graphical Abstract