Decorin attenuates hypertrophic scar fibrosis via TGFβ/Smad signalling.

The management of hypertrophic scars (HSs), characterized by excessive collagen production, involves various nonsurgical and surgical interventions. However, the absence of a well-defined molecular mechanism governing hypertrophic scarring has led to less-than-ideal results in clinical antifibrotic treatments. Therefore, our study focused on the role of decorin (DCN) and its regulatory role in the TGF-β/Smad signalling pathway in the development of HSs.

VGLL2 and TEAD1 fusion proteins drive YAP/TAZ-independent transcription and tumorigenesis by engaging p300.

Studies on Hippo pathway regulation of tumorigenesis largely center on YAP and TAZ, the transcriptional co-regulators of TEAD. Here, we present an oncogenic mechanism involving VGLL and TEAD fusions that is Hippo pathway-related but YAP/TAZ-independent. We characterize two recurrent fusions, VGLL2-NCOA2 and TEAD1-NCOA2, recently identified in spindle cell rhabdomyosarcoma.

NMT1 sustains ICAM-1 to modulate adhesion and migration of tumor cells.

Protein modifications have significant effects on tumorigenesis. N-Myristoylation is one of the most important lipidation modifications, and N-myristoyltransferase 1 (NMT1) is the main enzyme required for this process. However, the mechanism underlying how NMT1 modulates tumorigenesis remains largely unclear.

IGF2BP3 is an essential N-methyladenosine biotarget for suppressing ferroptosis in lung adenocarcinoma cells.

A lack of promising targets leads to poor prognosis in patients with lung adenocarcinoma (LUAD). Therefore, it is urgent to identify novel therapeutic targets. The importance of the N-methyladenosine (mA) RNA modification has been demonstrated in various types of tumors; however, knowledge of mA-related proteins in LUAD is still limited.

ISGylation of EMD promotes its interaction with PDHA to inhibit aerobic oxidation in lung adenocarcinoma.

Abnormal nuclear structure caused by dysregulation of skeletal proteins is a common phenomenon in tumour cells. However, how skeletal proteins promote tumorigenesis remains uncovered. Here, we revealed the mechanism by which skeletal protein Emerin (EMD) promoted glucose metabolism to induce lung adenocarcinoma (LUAD).

Tumour cells are sensitised to ferroptosis via RB1CC1-mediated transcriptional reprogramming.

Background: Ferroptosis, a form of regulated cell death, is an important topic in the field of cancer research. However, the signalling pathways and factors that sensitise tumour cells to ferroptosis remain elusive.

Methods: We determined the level of ferroptosis in cells by measuring cell death and lipid reactive oxygen species (ROS) production.

Essential roles of exosome and circRNA_101093 on ferroptosis desensitization in lung adenocarcinoma.

Background: Resistance to ferroptosis, a regulated cell death caused by iron-dependent excessive accumulation of lipid peroxides, has recently been linked to lung adenocarcinoma (LUAD). Intracellular antioxidant systems are required for protection against ferroptosis. The purpose of the present study was to investigate whether and how extracellular system desensitizes LUAD cells to ferroptosis.

YAP ISGylation increases its stability and promotes its positive regulation on PPP by stimulating 6PGL transcription.

Yes-associated protein (YAP) activation is crucial for tumor formation and development, and its stability is regulated by ubiquitination. ISGylation is a type of ubiquitination like post-translational modification, whereas whether YAP is ISGylated and how ISGylation influences YAP ubiquitination-related function remains uncovered. In addition, YAP can activate glucose metabolism by activating the hexosamine biosynthesis pathway (HBP) and glycolysis, and generate a large number of intermediates to promote tumor proliferation.

The essential roles of mA RNA modification to stimulate ENO1-dependent glycolysis and tumorigenesis in lung adenocarcinoma.

Background: Lung adenocarcinoma (LUAD)  is the most common subtype of lung cancer. Patient prognosis is poor, and the existing therapeutic strategies for LUAD are far from satisfactory. Recently, targeting N6-methyladenosine (mA) modification of RNA has been suggested as a potential strategy to impede tumor progression.

An Expectation Maximization Based Adaptive Group Testing Method for Improving Efficiency and Sensitivity of Large-Scale Screening of COVID-19.

The pathogen of the ongoing coronavirus disease 2019 (COVID-19) pandemic is a newly discovered virus called severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Testing individuals for SARS-CoV-2 plays a critical role in containing COVID-19. For saving medical personnel and consumables, many countries are implementing group testing against SARS-CoV-2.

tsRNA-5001a promotes proliferation of lung adenocarcinoma cells and is associated with postoperative recurrence in lung adenocarcinoma patients.

Background: The biological role and clinical significance of transfer RNA-derived small RNAs (tsRNAs) remain largely unclear. The purpose of this study was to investigate the biological function, molecular mechanism, and clinical significance of tsRNA-5001a in lung adenocarcinoma.

Methods: The function of tsRNA-5001a on the growth of tumor cells was accessed by cell function experiments.

Transcriptional Repression of Ferritin Light Chain Increases Ferroptosis Sensitivity in Lung Adenocarcinoma.

Ferroptosis is an iron- and lipid peroxidation-dependent form of regulated cell death. The release of labile iron is one of the important factors affecting sensitivity to ferroptosis. Yes-associated protein (YAP) controls intracellular iron levels by affecting the transcription of and .

TRIB2 desensitizes ferroptosis via βTrCP-mediated TFRC ubiquitiantion in liver cancer cells.

Tribbles homolog 2 (TRIB2) is known to boost liver tumorigenesis via regulating Ubiquitin (Ub) proteasome system (UPS). At least two ways are involved, i.e.

Targeting SLC3A2 subunit of system X is essential for mA reader YTHDC2 to be an endogenous ferroptosis inducer in lung adenocarcinoma.

The mA reader YT521-B homology containing 2 (YTHDC2) has been identified to inhibit lung adenocarcinoma (LUAD) tumorigenesis by suppressing solute carrier 7A11 (SLC7A11)-dependent antioxidant function. SLC7A11 is a major functional subunit of system X. Inhibition of system X can induce ferroptosis.

RRM2 protects against ferroptosis and is a tumor biomarker for liver cancer.

Background: Ferroptosis is the process of cell death triggered by lipid peroxides, and inhibition of glutathione (GSH) synthesis leads to ferroptosis. Liver cancer progression is closely linked to ferroptosis suppression. However, the mechanism by which inhibition of GSH synthesis suppresses potential ferroptosis of liver cancer cells and whether ferroptosis-related liver cancer biomarkers have a promising diagnostic value remain unknown.

Effect of TP53 rs1042522 on the susceptibility of patients to oral squamous cell carcinoma and oral leukoplakia: a meta-analysis.

Background: There are different and inconsistent conclusions regarding the genetic relationship between the human tumor suppressor p53 (TP53) rs1042522 polymorphism and the risk of oral squamous cell carcinoma (OSCC) and oral leukoplakia (OL). Therefore, the aim of the study was to comprehensively reassess this association through the performance of an updated meta-analysis.

Methods: After searching the available databases, we systematically screened and included the eligible case-control studies, which contain the full genotype frequency data of the TP53 rs1042522 polymorphism for both OSCC/OL patients and the negative control groups.

Predicting the progression of ophthalmic disease based on slit-lamp images using a deep temporal sequence network.

Ocular images play an essential role in ophthalmology. Current research mainly focuses on computer-aided diagnosis using slit-lamp images, however few studies have been done to predict the progression of ophthalmic disease. Therefore exploring an effective approach of prediction can help to plan treatment strategies and to provide early warning for the patients.

Automatic diagnosis of imbalanced ophthalmic images using a cost-sensitive deep convolutional neural network.

Background: Ocular images play an essential role in ophthalmological diagnoses. Having an imbalanced dataset is an inevitable issue in automated ocular diseases diagnosis; the scarcity of positive samples always tends to result in the misdiagnosis of severe patients during the classification task. Exploring an effective computer-aided diagnostic method to deal with imbalanced ophthalmological dataset is crucial.

Localization and diagnosis framework for pediatric cataracts based on slit-lamp images using deep features of a convolutional neural network.

Slit-lamp images play an essential role for diagnosis of pediatric cataracts. We present a computer vision-based framework for the automatic localization and diagnosis of slit-lamp images by identifying the lens region of interest (ROI) and employing a deep learning convolutional neural network (CNN). First, three grading degrees for slit-lamp images are proposed in conjunction with three leading ophthalmologists.

Inhibition of Bcl-2 potentiates AZD-2014-induced anti-head and neck squamous cell carcinoma cell activity.

Mammalian target of rapamycin (mTOR) is a therapeutic target for head and neck squamous cell carcinoma (HNSCC). Here, we evaluated the activity of AZD-2014, a potent mTOR complex 1/2 (mTORC1/2) dual inhibitor, against HNSCC cells. We showed that AZD-2014 blocked mTORC1/2 activation in established and primary human HNSCC cells, where it was anti-proliferative and pro-apoptotic.

[The preliminary study of the use of MRI navigation in identifying the safe surgical margin of the maxillofacial malignancy].

Objective: To evaluate the feasibility of MRI navigation in identifing the safe surgical margin of the maxillofacial malignancy.

Methods: The pathology results of the surgical margin identified by the technique of MRI navigation form 20 patients with maxillofacial malignancy were compared with those of 45 patients with maxillofacial malignancy who underwent the routine operation without MRI navigation.

Results: There was no difference between the two groups of patients in age, sex, size of tumor, tumor stages, pathologic diagnosis (P > 0.

The therapeutic effects of tectorigenin on chemically induced liver fibrosis in rats and an associated metabonomic investigation.

The aim of this study was to investigate the effects of tectorigenin on chemically induced liver fibrosis in rats. Liver fibrosis was induced in rats with carbon tetrachloride, a diet high in fat, cholesterol and alcohol in the drinking water. Our results indicate that tectorigenin treatment significantly inhibited the increases in the activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and the increases in the serum levels of hyaluronate (HA), laminin (LN) and procollagen III N-terminal peptide (PIIIP); tectorigenin treatment also significantly inhibited the increases in the amount of collagen in the livers of the fibrogenic rats.