https://nova.newcastle.edu.au/vital/access/ /manager/Index en-au 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:16707 Wed 11 Apr 2018 16:05:23 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14871 Wed 11 Apr 2018 10:34:19 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30150 Thu 17 Feb 2022 09:30:37 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:18436 Sat 24 Mar 2018 07:59:47 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:26890 Sat 24 Mar 2018 07:41:39 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38260 9-tetrahydrocannabinol (∆⁹-THC). Evidence is emerging for the therapeutic benefits of cannabis in the treatment of neurological and neurodegenerative diseases, with potential efficacy as an analgesic and antiemetic for the management of cancer-related pain and treatment-related nausea and vomiting, respectively. An increasing number of preclinical studies have established that ∆⁹-THC can inhibit the growth and proliferation of cancerous cells through the modulation of cannabinoid receptors (CB1R and CB2R), but clinical confirmation remains lacking. In parallel, the anti-cancer properties of non-THC cannabinoids, such as cannabidiol (CBD), are linked to the modulation of non-CB1R/CB2R G-protein-coupled receptors, neurotransmitter receptors, and ligand-regulated transcription factors, which together modulate oncogenic signalling and redox homeostasis. Additional evidence has also demonstrated the anti-inflammatory properties of cannabinoids, and this may prove relevant in the context of peritumoural oedema and the tumour immune microenvironment. This review aims to document the emerging mechanisms of anti-cancer actions of non-THC cannabinoids.]]> Mon 29 Jan 2024 17:45:13 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:42359 Mon 22 Aug 2022 14:08:27 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:39586 in silico using the Kaplan-Meier Plotter (n=3,935), the TCGA invasive breast carcinoma (n=960) and GOBO (n=821) data sets. Functional effects of BAALC expression on breast cancer proliferation, migration and invasion were determined in vitro. We demonstrate herein that BAALC expression is progressively increased in primary and breast cancer metastases when compared to normal breast tissue. Increased BAALC mRNA is associated with a reduction in DMFS and disease-free survival, but not OS, in breast cancer patients, even when corrected for tumor grade. We show that overexpression of BAALC in MCF-7 breast cancer cells increases the proliferation, anchorage-independent growth, invasion, and migration capacity of these cells. Conversely, siRNA knockdown of BAALC expression in Hs578T breast cancer cells decreases proliferation, invasion and migration. We identify that this BAALC associated migration and invasion is mediated by focal adhesion kinase (FAK)-dependent signaling and is accompanied by an increase in matrix metalloproteinase (MMP)-9 but not MMP-2 activity in vitro. Our data demonstrate a novel function for BAALC in the control of breast cancer metastasis, offering a potential target for the generation of anti-cancer drugs to prevent breast cancer metastasis.]]> Mon 08 Aug 2022 11:48:18 AEST ]]>