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Cancer: Skin Cancer
Therapy: Cancer Therapy

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Total 47 results found since Jan 2013.

Ferumoxytol- β-glucan Inhibits Melanoma Growth via Interacting with Dectin-1 to Polarize Macrophages into M1 Phenotype
Conclusion: The nanocomposite FMT-β-glucan suppressed melanoma growth by inducing the M1 macrophage-activated tumor microenvironment.PMID:34400883 | PMC:PMC8364471 | DOI:10.7150/ijms.61525
Source: International Journal of Medical Sciences - August 17, 2021 Category: Biomedical Science Authors: Xinghan Liu Yujun Xu Yi Li Yuchen Pan Shuli Zhao Yayi Hou Source Type: research

Cancers, Vol. 13, Pages 166: Molecular Targeting of HuR Oncoprotein Suppresses MITF and Induces Apoptosis in Melanoma Cells
Conclusion: HuR-NP exhibited antitumor activity in melanoma cells independent of their oncogenic B-RAF mutational status. Additionally, combinatorial therapy incorporating MEK inhibitor holds promise in overriding MITF-mediated drug resistance in melanoma.
Source: Cancers - January 6, 2021 Category: Cancer & Oncology Authors: Rebaz Ahmed Ranganayaki Muralidharan Akhil Srivastava Sarah E. Johnston Yan D. Zhao Suhendan Ekmekcioglu Anupama Munshi Rajagopal Ramesh Tags: Article Source Type: research

Abnormal overexpression of G9a in melanoma cells promotes cancer progression via upregulation of the Notch1 signaling pathway.
In this study, we first showed that G9a was significantly upregulated in melanoma patients. Using the TCGA database, we found a significantly higher expression of G9a in primary melanoma samples (n = 461) compared to normal skin samples (n = 551). Next, we knocked down G9a in human M14 and A375 melanoma cell lines in vitro via small interfering RNA (siRNA). This resulted in a significant decrease in cell viability, migration and invasion, and an increase in cell apoptosis. UNC0642 is a small molecule inhibitor of G9a that demonstrates minimal cell toxicity and good in vivo pharmacokinetic characteristics. We investigated t...
Source: Aging - February 2, 2020 Category: Biomedical Science Authors: Dang NN, Jiao J, Meng X, An Y, Han C, Huang S Tags: Aging (Albany NY) Source Type: research

Downregulation of MUTYH contributes to cisplatin ‑resistance of esophageal squamous cell carcinoma cells by promoting Twist‑mediated EMT.
In conclusion, the present data demonstrated that EMT activation mediated by MUTYH downregulation, by both enhancing Twist transcription and blocking its degradation, is one of the mechanisms for acquisition of CDDP resistance in ESCC. PMID: 31578574 [PubMed - as supplied by publisher]
Source: Oncology Reports - October 4, 2019 Category: Cancer & Oncology Tags: Oncol Rep Source Type: research

microRNA-374 inhibits proliferation and promotes apoptosis of mouse melanoma cells by inactivating the Wnt signalling pathway through its effect on tyrosinase.
Abstract Melanoma is one of the most malignant skin tumours with constantly increasing incidence worldwide. Previous studies have demonstrated that microRNA-374 (miR-374) is a novel biomarker for cancer therapy. Therefore, this study explores whether miR-374 targeting tyrosinase (TYR) affects melanoma and its underlying mechanism. We constructed subcutaneous melanoma models to carry out the following experiments. The cells were transfected with a series of miR-374 mimics, miR-374 inhibitors or siRNA against TYR. Dual luciferase reporter gene assay was used for the verification of the targeting relationship between...
Source: J Cell Mol Med - June 16, 2019 Category: Molecular Biology Authors: Li XJ, Li ZF, Xu YY, Han Z, Liu ZJ Tags: J Cell Mol Med Source Type: research

Detailed Dissection of UBE3A-Mediated DDI1 Ubiquitination
Discussion Poly-ubiquitinated proteins targeted for degradation might be recognized directly by proteasomal receptors or by proteasomal shuttling proteins. The first shuttling proteins – Ddi1, Rad23 and Dsk2 – were identified and characterized in Saccharomyces cerevisiae (Lambertson et al., 1999; Kaplun et al., 2005). Proteasomal shuttles contain an N-terminal ubiquitin-like (UBL) domain that interacts with the 26S proteasome (Finley, 2009), and a C-terminal ubiquitin-binding domain domain (UBD) that binds to ubiquitin or poly-ubiquitin chains (Bertolaet et al., 2001). When ubiquitinated, substrates are capt...
Source: Frontiers in Physiology - May 2, 2019 Category: Physiology Source Type: research

Non-canonical Notch Signaling Regulates Actin Remodeling in Cell Migration by Activating PI3K/AKT/Cdc42 Pathway
In conclusion, our research results indicate that DAPT activates PI3K/AKT/Cdc42 signaling by non-canonical Notch pathway, and the activated Cdc42 promotes the filopodia formation and inhibits lamellipodia assembly, resulting in reduced migration of breast cancer cells. The results imply that non-canonical Notch signaling may play a very important role in the rapid response of cells to the extracellular signals. Author Contributions LG, JD, and LL designed the study and wrote and revised the manuscript. LL and LZ performed most of the experiments and data analysis. SZ, X-YZ, P-XM, Y-DM, Y-YW, YC, S-JT, and Y-JZ assisted i...
Source: Frontiers in Pharmacology - April 15, 2019 Category: Drugs & Pharmacology Source Type: research

Connecting Metainflammation and Neuroinflammation Through the PTN-MK-RPTP β/ζ Axis: Relevance in Therapeutic Development
Conclusion The expression of the components of the PTN-MK-RPTPβ/ζ axis in immune cells and in inflammatory diseases suggests important roles for this axis in inflammation. Pleiotrophin has been recently identified as a limiting factor of metainflammation, a chronic pathological state that contributes to neuroinflammation and neurodegeneration. Pleiotrophin also seems to potentiate acute neuroinflammation independently of the inflammatory stimulus while MK seems to play different -even opposite- roles in acute neuroinflammation depending on the stimulus. Which are the functions of MK and PTN in chronic neuroi...
Source: Frontiers in Pharmacology - April 11, 2019 Category: Drugs & Pharmacology Source Type: research

Hepatoma-Derived Growth Factor and DDX5 Promote Carcinogenesis and Progression of Endometrial Cancer by Activating β-Catenin
Conclusion: Our results provide novel evidence that HDGF interacts with DDX5 and promotes the progression of EC through the induction of β-catenin. Introduction Endometrial cancer (EC) comprises the most common malignancy involving the female genital tract and the fourth most common malignancy in women after breast, lung, and colorectal cancers (1). In 2012, approximately 320,000 new cases of EC were diagnosed worldwide and the incidence is increasing (2). Currently, endometrial carcinogenesis is thought to be a multi-step process involving the coordinated interaction of hormonal regulation, gene mutation, ad...
Source: Frontiers in Oncology - April 10, 2019 Category: Cancer & Oncology Source Type: research

Complement C5b-9 and Cancer: Mechanisms of Cell Damage, Cancer Counteractions, and Approaches for Intervention
In conclusion, osmotic burst of inflated complement-damaged cells may occur, but these bursts are most likely a consequence of metabolic collapse of the cell rather than the cause of cell death. The Complement Cell Death Mediator: A Concerted Action of Toxic Moieties Membrane pores caused by complement were first visualized by electron microscopy on red blood cell membranes as large ring structures (22). Similar lesions were viewed on E. coli cell walls (23). Over the years, ample information on the fine ultrastructure of the MAC that can activate cell death has been gathered (24) and has been recently further examined (...
Source: Frontiers in Immunology - April 9, 2019 Category: Allergy & Immunology Source Type: research

Co-targeting PLK1 and mTOR induces synergistic inhibitory effects against esophageal squamous cell carcinoma
In this study, we found that suppression of PLK1 by specific siRNA or inhibitor attenuated mTOR activity in ESCC cells. Phosphorylated S6, a downstream effector of mTOR signaling, was significantly correlated with overexpression of PLK1 in a subset of ESCC. These data suggest that PLK1 activates mTOR signaling in vitro and in vivo. More importantly, the mTOR inhibitor rapamycin synergized with PLK1 inhibitor BI 2536 to inhibit ESCC cell proliferation in culture and in mice. Notably, combined treatment with BI 2536 and rapamycin produced more potent inhibitory effects on the activation of S6 and AKT than either alone. Furth...
Source: Journal of Molecular Medicine - June 29, 2018 Category: Molecular Biology Source Type: research

Aquaporin-1 inhibition reduces metastatic formation in a mouse model of melanoma.
In conclusion, these findings highlight an additional role for AQP1 as an important determinant of tumour dissemination by facilitating tumour cell extravasation and metastatic formation. This study adds knowledge on the role played by AQP1 in tumour biology and supports the view of AQP1 as a potential drug target for cancer therapy. PMID: 29044946 [PubMed - as supplied by publisher]
Source: J Cell Mol Med - October 17, 2017 Category: Molecular Biology Authors: Simone L, Gargano CD, Pisani F, Cibelli A, Mola MG, Frigeri A, Svelto M, Nicchia GP Tags: J Cell Mol Med Source Type: research

Aquaporin ‐1 inhibition reduces metastatic formation in a mouse model of melanoma
In conclusion, these findings highlight an additional role for AQP1 as an important determinant of tumour dissemination by facilitating tumour cell extravasation and metastatic formation. This study adds knowledge on the role played by AQP1 in tumour biology and supports the view of AQP1 as a potential drug target for cancer therapy.
Source: Journal of Cellular and Molecular Medicine - October 1, 2017 Category: Molecular Biology Authors: Laura Simone, Concetta Domenica Gargano, Francesco Pisani, Antonio Cibelli, Maria Grazia Mola, Antonio Frigeri, Maria Svelto, Grazia Paola Nicchia Tags: Original Article Source Type: research

BRCA2 protects mammalian cells from heat shock.
CONCLUSION: BRCA2 has a protecting role against heat-induced cell death. BRCA2 might be a potential molecular target for hyperthermic cancer therapy. PMID: 28891354 [PubMed - as supplied by publisher]
Source: International Journal of Hyperthermia - September 13, 2017 Category: Internal Medicine Tags: Int J Hyperthermia Source Type: research

ZIC5 Drives Melanoma Aggressiveness by PDGFD-Mediated Activation of FAK and STAT3
Insights into mechanisms of drug resistance could extend the efficacy of cancer therapy. To probe mechanisms in melanoma, we performed siRNA screening of genes that mediate the development of neural crest cells, from which melanocytes are derived. Here, we report the identification of ZIC5 as a mediator of melanoma drug resistance. ZIC5 is a transcriptional suppressor of E-cadherin expressed highly in human melanoma. ZIC5 enhanced melanoma cell proliferation, survival, drug resistance, in vivo growth and metastasis. Microarray analysis revealed that ZIC5 downstream signaling included PDGFD and FAK activation, which contrib...
Source: Cancer Research - January 15, 2017 Category: Cancer & Oncology Authors: Reiko Satow, Tomomi Nakamura, Chiaki Kato, Miku Endo, Mana Tamura, Ryosuke Batori, Shiori Tomura, Yumi Murayama, Kiyoko Fukami Tags: Molecular and Cellular Pathobiology Source Type: research