Melanoma is a disease with a high recurrence rate and poor prognosis; therefore, the need for targeted therapeutics is steadily increasing. Oligodendrocyte transcription factor2 (Olig2) is a basic helix-loop-helix transcription factor that is expressed in the central nervous system during embryonic development. Olig2 is overexpressed in various malignant cell lines such as lung carcinoma, glioma and melanoma. Olig2 is known as a key transcription factor that promotes tumor growth in malignant glioma. However, the role of Olig2 in melanoma is not well characterized. We analyzed the role of Olig2 in apoptosis, migration, and invasion of melanoma cells. We confirmed that Olig2 was overexpressed in melanoma cells and tissues. Reduction of Olig2 increased apoptosis in melanoma cells by increasing p53 level and caspase-3/-7 enzyme activity. In addition, downregulation of Olig2 suppressed migration and invasion of melanoma cells by inhibiting EMT. Reduction of Olig2 inhibited expression of MMP-1 and the enzyme activity of MMP-2/-9 induced by TGF-β. Moreover, Olig2 was involved in the downstream stages of MEK/ERK and PI3K/AKT, which are major signaling pathways in metastatic progression of melanoma. In conclusion, this study demonstrated the crucial roles of Olig2 in apoptosis, migration, and invasion of melanoma and may help to further our understanding of the relationship between Olig2 and melanoma progression.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8032681 | PMC |
| http://dx.doi.org/10.1038/s41598-021-87438-x | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
CD93 blockade promotes effector T-cell infiltration and facilitates adoptive cell therapy in solid tumors.
J Immunother Cancer
January 2025
Division of Surgical Oncology, Department of Surgery, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA
Background: Adaptive cellular therapy (ACT), particularly chimeric antigen receptor (CAR)-T cell therapy, has been successful in the treatment of hemopoietic malignancies. However, poor trafficking of administered effector T cells to the tumor poses a great hurdle for this otherwise powerful therapeutic approach in solid cancers. Our previous study revealed that targeting CD93 normalizes tumor vascular functions to improve immune checkpoint blockade therapy.
View Article and Find Full Text PDFCryoshocked Adipocytes Mediated Dual-Modal Strategy Combining Photodynamic Therapy and Triptolide Palmitate for Pulmonary Metastatic Melanoma Treatment.
Adv Sci (Weinh)
January 2025
Department of Pharmacy, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Pulmonary metastasis represents one of the most prevalent forms of metastasis in advanced melanoma, with mortality rates reaching 70%. Current treatments including chemotherapy, targeted therapy, and immunotherapy frequently exhibit limited efficacy or present high costs. To address these clinical needs, this study presents a biomimetic drug delivery system (Ce6-pTP-CsA) utilizing cryoshocked adipocytes (CsA) encapsulating the prodrug triptolide palmitate (pTP) and the photosensitizer Ce6, exploiting the characteristic of tumor cells to recruit and lipolyze adipocytes for energy.
View Article and Find Full Text PDFLoss of NF1 accelerates uveal and intra-dermal melanoma tumorigenesis and oncogenic GNAQ transforms Schwann cells.
Cancer Res Commun
January 2025
University of British Columbia, Vancouver, BC, Canada.
NF1 encodes the multifunctional tumour suppressor protein, neurofibromin, which is best known for its causative role in Neurofibromatosis type 1 and in regulating MAPK signaling. Neurofibromin, in a context-specific manner, is involved in various tumorigenic processes, including those in melanocytes. This study investigated whether NF1 loss can collaborate with oncogenic GNAQ to promote melanoma in the dermis or eyes, where the G alpha q pathway is almost always activated.
View Article and Find Full Text PDFRET Inhibitor SPP86 Triggers Apoptosis and Activates the DNA Damage Response Through the Suppression of Autophagy and the PI3K/AKT Signaling Pathway in Melanoma Cells.
Drug Des Devel Ther
January 2025
The Key Laboratory of Molecular Pharmacology, Liaocheng People's Hospital, Liaocheng, Shandong, People's Republic of China.
Background: Melanoma is a highly lethal form of skin cancer, and effective treatment remains a significant challenge. SPP86 is a novel potential therapeutic drug. Nonetheless, the specific influence of SPP86 on autophagy, particularly its mechanisms in the context of DNA damage and apoptosis in human melanoma cells, remains inadequately understood.
View Article and Find Full Text PDFCells under high confinement form highly polarized hydrostatic pressure-driven, stable leader blebs that enable efficient migration in low adhesion, environments. Here we investigated the basis of the polarized bleb morphology of metastatic melanoma cells migrating in non-adhesive confinement. Using high-resolution time-lapse imaging and specific molecular perturbations, we found that EGF signaling via PI3K stabilizes and maintains a polarized leader bleb.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!