CHD1L accelated the progression of cutaneous squamous cell carcinoma via promoting PI3K/PD-L1 signaling pathway induced M2 polarization of TAMs.

To investigate CHD1L's impacts and molecular processes in hypoxic cutaneous squamous cell carcinoma. Monoclonal proliferation assays and CCK-8 were used to detect the proliferation capacity of A431 cells and Colon16 cells; wound healing experiments and Transwell assays were used to examine the migration and invasion capacity of A431 cells and Colon16 cells; angiogenesis experiments were conducted to assess the influence of A431 cells on angiogenesis; a nude mouse tumor xenograft experiment and HE staining were utilized to evaluate the impact of CHD1L on the progression of cutaneous squamous cell carcinoma; western blot analysis was performed to detect the expression of p-PI3K, p-AKT, and PD-L1 in A431 cells, as well as CD9, TSG101, PD-L1 in exosomes, and CD206, Arginase-1, iNOS, IL-1β, p-AKT, p-mTOR, VEGF, COX-2, MMP2, MMP9, p-ERK1/2 in tumor-associated macrophages. Under hypoxic conditions, CHD1L promoted the proliferation, migration, invasion, and angiogenesis of cutaneous squamous cell carcinoma.

Gamma-glutamyl transpeptidase and indirect bilirubin may participate in systemic inflammation of patients with psoriatic arthritis.

Background: Previous studies have suggested that systemic metabolic abnormalities are closely related to psoriatic arthritis (PsA). Gamma-glutamyl transpeptidase (GGT) and indirect bilirubin (IBIL), two essential active substances in hepatic metabolism that have been demonstrated as an oxidative and anti-oxidative factor respectively, have been proved to be involved in oxidative stress damage and inflammation in several human diseases. However, their role in PsA remains unclear.

Corrigendum: Dihydrocapsaicin inhibits cell proliferation and metastasis in melanoma down-regulating β-catenin pathway.

[This corrects the article DOI: 10.3389/fonc.2021.

ZC3H15 Correlates with a Poor Prognosis and Tumor Progression in Melanoma.

Zinc figure CCCH-type containing 15 (ZC3H15), also called developmentally regulated GTP-binding protein 1 (DRG1) family regulatory protein 1 (DFRP1), is a zinc finger containing protein. Despite playing a role in cellular signaling, it is found overexpressed in acute myeloid leukemia and also an independent prognostic marker in hepatocellular carcinoma patients. However, the biological effect of ZC3H15 in malignant melanoma (MM) remains unexplored.

Dihydrocapsaicin Inhibits Cell Proliferation and Metastasis in Melanoma Down-regulating β-Catenin Pathway.

Dihydrocapsaicin (DHC) is one of the main components of capsaicinoids in Capsicum. It has been reported that DHC exerts anti-cancer effects on diverse malignant tumors, such as colorectal cancer, breast cancer, and glioma. However, studies focused on the effect of DHC upon melanoma have rarely been done.

CSN6 promotes melanoma proliferation and metastasis by controlling the UBR5-mediated ubiquitination and degradation of CDK9.

As a critical subunit of the constitutive photomorphogenesis 9 (COP9) signalosome (CSN), CSN6 is upregulated in some human cancers and plays critical roles in tumorigenesis and progression, but its biological functions and molecular mechanisms in melanoma remain unknown. Our study showed that CSN6 expression was upregulated in melanoma patients and cells, and correlated with poor survival in melanoma patients. In melanoma cells, CSN6 knockdown remarkably inhibited cell proliferation, tumorigenicity, migration, and invasion, whereas CSN6 recovery rescued the proliferative and metastatic abilities.

Dehydrocorydaline inhibits cell proliferation, migration and invasion via suppressing MEK1/2-ERK1/2 cascade in melanoma.

Alkaloids are naturally occurring chemical compounds that are widely distributed in plants, and have pharmaceutical values and low toxicity. In recent years, some of them have been demonstrated to be promising therapeutic drug candidates for cancer treatment. Herein, we tried to explore the antitumor effect of dehydrocorydaline (DHC), a natural alkaloid isolated from , on malignant melanoma.

Fatal Vitamin K-Dependent Coagulopathy Associated with Cefoperazone/Sulbactam: A Case Report.

This case report describes a suspected and fatal adverse reaction involving vitamin K-dependent coagulopathy that might be associated with cefoperazone/sulbactam (CPZ/SAM), a combined antimicrobial formulation. We reported a patient diagnosed with acute cerebral infarction and secondary pulmonary infection who was treated with an intravenous infusion of CPZ/SAM at 3 g twice daily. After receiving treatment with CPZ/SAM, the patient developed a fatal adverse reaction of CPZ-induced hemorrhage.

Inactivation/deficiency of DHODH induces cell cycle arrest and programed cell death in melanoma.

Malignant melanoma (MM) is one of the most malignant tumors and has a very poor prognosis. However, there are no effective drugs to treat this disease. As a kind of iron flavin dependent enzyme, dihydroorotate dehydrogenase (DHODH, EC 1.

Function and mechanism of neurotensin (NTS) and its receptor 1 (NTSR1) in occurrence and development of tumors.

As a neuropeptide, neurotensin (NTS) is widely expressed in central and peripheral nervous system, which is mainly mediated byneurotensin receptor1 (NTSR1) to activate the related downstream signaling pathways. After summarized the function and mechanism of NTS/NTSR1 in various malignant tumors, we found that NTS/NTSR1 played essential roles during tumor initiation and development. NTS/NTSR1 regulates tumor initiation, proliferation, apoptosis, metastasis and differentiation mainly through three pathways, including IP3/Ca2+ /PKC/MAPKs pathway, MMPs/EGFR/MAPKs (PI3K/Akt) pathway, or Rho-GTPsaes and non-receptor tyrosine kinase pathway.

Antibiotic drug tigecycline inhibits melanoma progression and metastasis in a p21CIP1/Waf1-dependent manner.

Antibiotics are common drugs with low toxicity but high effectiveness. They have been suggested to be drug candidates for cancer therapy in recent years. Here, we tried to investigate the antitumour effect of tigecycline on malignant melanoma.