A5056721236- RNA modifications and cancer
- Cancer-related gene regulation
- HVDC Systems and Fault Protection
- Hippo pathway signaling and YAP/TAZ
- Cancer-related molecular mechanisms research
- Synthesis and biological activity
- Click Chemistry and Applications
- Cytokine Signaling Pathways and Interactions
- Ubiquitin and proteasome pathways
- Plant Surface Properties and Treatments
- Photodynamic Therapy Research Studies
- Peptidase Inhibition and Analysis
- Immune Cell Function and Interaction
- Retinoids in leukemia and cellular processes
- Melanoma and MAPK Pathways
- Galectins and Cancer Biology
- Bioactive Compounds and Antitumor Agents
- RNA and protein synthesis mechanisms
- Wnt/β-catenin signaling in development and cancer
- Cellular Mechanics and Interactions
- Cancer Mechanisms and Therapy
- Signaling Pathways in Disease
- Immune cells in cancer
- Psoriasis: Treatment and Pathogenesis
- Reproductive System and Pregnancy
Chosun University
2019-2024
IL-34 has been recently identified as a ligand for CSF1R that regulates various cellular processes including cell proliferation, survival, and differentiation. Although the binding of to modulates several cancer-driving signaling pathways, little is known about role IL-34/CSF1R in breast cancer. Herein, we report induces epithelial transformation tumorigenesis through activation MEK/ERK JNK/c-Jun pathways. increased phosphorylation MEK1/2, ERK1/2, JNK1/2, c-Jun mouse skin epidermal JB6 C141...
Reversible N6-adenosine methylation of mRNA, referred to as m6A modification, has emerged an important regulator post-transcriptional RNA processing. Numerous studies have highlighted its crucial role in the pathogenesis diverse diseases, particularly cancer. Post-translational modifications m6A-related proteins play a fundamental regulating methylome, thereby influencing fate m6A-methylated RNA. A comprehensive understanding mechanisms that regulate and factors contributing specificity...
Given the increasing recognition of relationship between IL-1 cytokines, inflammation, and cancer, significance distinct members cytokine family in etiology cancer has been widely researched. In present study, we investigated underlying mechanism IL-36γ/IL-36R axis during breast progression, which not yet elucidated. Initially, determined effects IL-36γ on proliferation epithelial cell transformation JB6 Cl41 mouse epidermal MCF7 human cells using BrdU incorporation anchorage-independent...
Background/Aim: Triple negative breast cancer (TNBC) is an aggressive type of with limited targets for chemotherapy. This study evaluated the inhibitory effects novel imidazo[2,1-b]oxazole-based rapidly accelerated fibrosarcoma (RAF) inhibitors, KIST0215-1 and KIST0215-2, on epithelial cell transformation TNBC tumorigenesis. Materials Methods: Immunoblotting, BrdU incorporation assay, reporter gene soft agar assay analyses were performed. In vivo studied using BALB/c mouse xenograft model....
PLX4032 is commonly used in the treatment of advanced melanoma patients with BRAF-V600E mutation. The aim this study was to elucidate mechanisms by which up-regulation PIN1 confers resistance melanoma.The expression as well cytotoxic effects combinatorial and all-trans retinoic acid (ATRA) were investigated immunoblotting, MTT assay, TUNEL soft agar assay.PIN1 up-regulated A375R cells, a PLX4032-resistant subline cells generated from an A375 cell line, compared parental cells. Indeed,...
The B-raf proto-oncogene, serine/threonine kinase (BRAF) V600E mutation is frequent in patients with advanced melanoma. PLX4032, an inhibitor of BRAFV600E kinase, effective for the treatment melanoma BRAF V600E-positive patients; however, resistance eventually develops due to paradoxical activation mitogen-activated protein (MEK)/extracellular signal-regulated kinases (ERK) pathway resulting from RAF dimerization. In this study, we investigated inhibitory effects a novel...
Although N 6 -adenosine methyltransferase (METTL3) is frequently upregulated in breast cancer patients, the anticancer effect of small-molecule inhibitors targeting METTL3 has not yet been studied.The present study aimed to investigate anti-tumorigenic effects STM2457, a inhibitor, on panel cells representing distinct clinical subtypes.Measurement cell viability using MTT assay demonstrated dose-and time-dependent reduction MCF7, SKBR3, and MDA-MB-231 cells, which are representative luminal...
Abstract Nuclear accumulation of YAP/TAZ promotes tumorigenesis in several cancers, including melanoma. Although the underlying mechanisms for nuclear retention YAP are known, those responsible TAZ remain unclear. We aimed to evaluate role a novel acetylation/deacetylation switch that regulates its subcellular localization lung metastasis melanoma cells. CREB binding protein (CBP) mediated acetylation at K54 response stimulation with epidermal growth factor or transforming beta whereas...
Abstract Methyltransferase-like 3 (METTL3) is the catalytic subunit of N 6 -adenosine methyltransferase complex responsible for -methyladenosine (m A) modification mRNA in mammalian cells. Although METTL3 expression increased several cancers, regulatory mechanisms are unclear. We explored roles peptidyl-prolyl cis-trans isomerase NIMA-interacting 1 (PIN1) stability and m6A mRNA. PIN1 interacted with prevented its ubiquitin-dependent proteasomal lysosomal degradation. It stabilized METTL3,...