WISP1 Inhibits Hepatocellular Carcinoma Cell Proliferation by Promoting CyclinD1 Ubiquitination and Downregulating its Expression.

Hepatocellular carcinoma (HCC), a leading cause of cancer-related deaths, is often linked to dysregulated cell cycle proteins. This study focuses on the role of WISP1 in modulating Cyclin D1, a key cell cycle regulator, in HCC. The study used HCCLM3 and Hep3B cells to assess the expression of Cyclin D1 and cell proliferation following the treatment of WISP1.

A rare perspective: fine-needle aspiration cytologic features of hyaline vascular type of Castleman disease: A case report.

Rationale: Castleman disease, also known as Castleman syndrome, is a rare, nonmalignant lymphoproliferative disorder. The localized subtype of this disease is primarily the hyaline vascular type of Castleman disease (HVCD). Although this disease is a benign lesion, the histologic features are similar to those of some malignant lymphomas, so an accurate diagnosis of the disease is required.

USP22 Promotes Osteosarcoma Progression by Stabilising β-Catenin and Upregulating HK2 and Glycolysis.

Osteosarcoma is a primary malignancy that is difficult to treat and is prone to developing resistance to chemotherapy. As such, it is necessary to continuously explore novel therapeutic targets. Ubiquitin-specific protease 22 (USP22) is an ubiquitin-specific protease that has been demonstrated to have potent carcinogenic effects on a variety of cancers and is involved in several biological processes.

Deubiquitinase USP10 promotes osteosarcoma autophagy and progression through regulating GSK3β-ULK1 axis.

Background: Deubiquitinating enzymes (DUBs) are pivotal in maintaining cell homeostasis by regulating substrate protein ubiquitination in both healthy and cancer cells. Ubiquitin-specific protease 10 (USP10) belongs to the DUB family. In this study, we investigated the clinical and pathological significance of USP10 and Unc-51-like autophagy activating kinase 1 (ULK1) in osteosarcoma (OS), as well as the mechanism of USP10 action in ULK1-mediated autophagy and disease progression.

Warning Function of Frank's Sign in Pre-Existing Cardiac Disease Patients: A Case Report.

Frank's sign (FS) refers to a diagonal skin fold between the tragus and the outer edge of the earlobe. FS has been identified as an independent variable in coronary artery disease (CAD). Young patients with FS and previous myocardial infarction are still rarely reported in clinical studies.

Vaginal microbiota: Potential targets for vulvovaginal candidiasis infection.

Vulvovaginal candidiasis (VVC) is the second most common cause of vaginal infection globally after bacterial vaginosis (BV) and associated with adverse reproductive and obstetric outcomes, including preterm delivery, sexually transmitted infections and pelvic inflammatory disease. Although effective control of VVC is achievable with the use of traditional treatment strategies (i.e.

Comparison of serum from lung cancer patients and from patients with benign lung nodule using FTIR spectroscopy.

Lungcancer remains the leading cause of cancer related deaths in worldwide. Earlydiagnosis oflungcancer can significantly improve survival rate. However, due to its close resemblance to the malignant nodules, the possible existence of benign nodules often leads to erroneous decisions.

Tea domain transcription factor TEAD4 mitigates TGF-β signaling and hepatocellular carcinoma progression independently of YAP.

Tea domain transcription factor 4 (TEAD4) plays a pivotal role in tissue development and homeostasis by interacting with Yes-associated protein (YAP) in response to Hippo signaling inactivation. TEAD4 and YAP can also cooperate with transforming growth factor-β (TGF-β)-activated Smad proteins to regulate gene transcription. Yet, it remains unclear whether TEAD4 plays a YAP-independent role in TGF-β signaling.

Phosphorylation of enteroviral 2A at Ser/Thr125 benefits its proteolytic activity and viral pathogenesis.

Enteroviral 2A proteinase (2A ), a well-established and important viral functional protein, plays a key role in shutting down cellular cap-dependent translation, mainly via its proteolytic activity, and creating optimal conditions for Enterovirus survival. Accumulated data show that viruses take advantage of various signaling cascades for their life cycle; studies performed by us and others have demonstrated that the extracellular signal-regulated kinase (ERK) pathway is essential for enterovirus A71 (EV-A71) and other viruses replication. We recently showed that ERK1/2 is required for the proteolytic activity of viral 2A ; however, the mechanism underlying the regulation of 2A remains unknown.

Ubiquitin-like protein FAT10 promotes renal fibrosis by stabilizing USP7 to prolong CHK1-mediated G2/M arrest in renal tubular epithelial cells.

Renal fibrosis is the pathological hallmark of chronic kidney disease that is influenced by numerous factors. Arrest of renal tubular epithelial cells (RTECs) in G2/M phase is closely correlated with the progression of renal fibrosis; however, the mechanisms mediating these responses remain poorly defined. In this study, we observed that human leukocyte antigen-F adjacent transcript 10 (FAT10) deficiency abolished hypoxia-induced upregulation of checkpoint kinase 1 (CHK1) expression in RTECs derived from FAT10 and FAT10 mice.

NR3C2 suppresses the proliferation, migration, invasion and angiogenesis of colon cancer cells by inhibiting the AKT/ERK signaling pathway.

Nuclear receptor subfamily 3, group C, member 2 (NR3C2) serves an antitumorigenic role in several types of cancer; however, its role and mechanisms of action in colon cancer remains to be elucidated. The aim of the present study was to explore the effects of NR3C2 on the proliferation, migration, invasion and angiogenesis of colon cancer cells. The expression levels of NR3C2 in human colon epithelial NCM460 cells (spontaneously immortalized cell line) and colon cancer cell lines was detected using reverse transcription‑quantitative PCR and western blotting.

Inonotus obliquus polysaccharides induces apoptosis of lung cancer cells and alters energy metabolism via the LKB1/AMPK axis.

The present study explores the mechanisms underlying the anti-cancer action of Inonotus obliquus polysaccharides (IOP). Thus, we characterized the IOP components extracted from Chaga sclerotium and, found that the extracts contained 70% polysaccharides with an average molecular weight of 4.5 × 10 Da consisting of 75% glucose.

Dual Roles of the AMP-Activated Protein Kinase Pathway in Angiogenesis.

Angiogenesis plays important roles in development, stress response, wound healing, tumorigenesis and cancer progression, diabetic retinopathy, and age-related macular degeneration. It is a complex event engaging many signaling pathways including vascular endothelial growth factor (VEGF), Notch, transforming growth factor-beta/bone morphogenetic proteins (TGF-β/BMPs), and other cytokines and growth factors. Almost all of them eventually funnel to two crucial molecules, VEGF and hypoxia-inducing factor-1 alpha (HIF-1α) whose expressions could change under both physiological and pathological conditions.

AMP-activated protein kinase regulates cancer cell growth and metabolism via nuclear and mitochondria events.

Adenine monophosphate-activated protein kinase (AMPK) is a fuel sensing enzyme that is activated in shortage of energy and inhibited in its surplus. Cancer is a metabolic disease characteristic of aerobic glycolysis, namely Warburg effect, and possesses heterogeneity featured by spatiotemporal hypoxia and normoxia, where AMPK is deeply implicated. The present study delineates the regulation of mitochondrial functions by AMPK in cancer cells.

Negative regulation of TGF-β by AMPK and implications in the treatment of associated disorders.

Transforming growth factor beta (TGF-β) regulates a large number of biological processes, including proliferation, differentiation, immune response, and development. In addition, TGF-β plays important roles in some pathological processes, for instance, it is upregulated and activated in fibrosis and advanced cancer. Adenosine monophosphate-activated protein kinase (AMPK) acts as a fuel gauge that is activated when cells sense shortage of ATP and increase in AMP or AMP:ATP ratio.

Phosphatidylethanolamine binding protein 4 (PEBP4) is a secreted protein and has multiple functions.

Phosphatidylethanolamine binding proteins (PEBP) represent a superfamily of proteins that are conserved from bacteria to humans. In mammals, four members have been identified, PEBP1-4. To determine the functional differences among PEBP1-4 and the underlying mechanism for their actions, we performed a sequence alignment and found that PEBP4 contains a signal peptide and potential glycosylation sites, whereas PEBP1-3 are intracellular proteins.