The attachment of cells to the extracellular matrix (ECM) is the hallmark of structure–function stability and well-being. ECM detachment in localized tumors precedes abnormal dissemination of tumor cells culminating in metastasis. Programmed cell death (PCD) is activated during tumorigenesis to clear off ECM-detached cells through “anoikis.” However, cancer cells develop several mechanisms for abrogating anoikis, thus promoting their invasiveness and metastasis. Specific factors, such as growth proteins, pH, transcriptional signaling pathways, and oxidative stress, have been reported as drivers of anoikis resistance, thus enhancing cancer proliferation and metastasis. Recent studies highlighted the key contributions of metabolic pathways, enabling the cells to bypass anoikis. Therefore, understanding the mechanisms driving anoikis resistance could help to counteract tumor progression and prevent metastasis. This review elucidates the dynamics employed by cancer cells to impede anoikis, thus promoting proliferation, invasion, and metastasis. In addition, the authors have discussed other metabolic intermediates (especially amino acids and nucleotides) that are less explored, which could be crucial for anoikis resistance and metastasis.

Myeloid-derived suppressor cells (MDSCs) play crucial roles in tumorigenesis and their inhibition is critical for successful cancer immunotherapy. MDSCs undergo metabolic reprogramming from glycolysis to fatty acid oxidation (FAO) and oxidative phosphorylation led by lipid accumulation in tumor. Increased exogenous fatty acid uptake by tumor MDSCs enhance their immunosuppressive activity on T-cells thus promoting tumor progression. Tumor-infiltrating MDSCs in mice may prefer FAO over glycolysis as a primary source of energy while treatment with FAO inhibitors improved anti-tumor immunity. This review highlights the immunosuppressive functions of lipid metabolism and its signaling pathways on MDSCs in the tumor microenvironment. The manipulation of these pathways in MDSCs is relevant to understand the tumor microenvironment therefore, could provide novel therapeutic approaches to enhance cancer immunotherapy.

Plants and plant products are continuously being explored in medicine against the increasing number of antibiotic resistant organisms. The antimicrobial activity of essential oil of some plants has been demonstrated against a range of organism. This study aimed to determine the chemical constituents and the antimicrobial effects of the oil of grape peels on some clinical isolates. The oil was obtained from the peels by hydrodistillation procedure and analyzed using Gas chromatography coupled to mass spectrometer. The in-vitro antimicrobial property of the methanolic, ethanolic and tween 80 mixture of extract was determined by agar well diffusion method against selected clinical bacterial isolates (Bacillus cereus, Enterococcus faecalis, Escherichia coli, E. coli ATCC 25292, Klebsellia pneumonia, Pseudococcus sp., Salmonella typhmurium, Shigella flexneri, Staphylococcus aureus, Staphylococus aureus ATCC 29213) and fungal isolates (Aspergillus niger, Candida albican, and Penicillium chrysogenum). The GC-MS analyses of the oil indicated the amount of the essential oil components was highest with D-Limonene (75.05%), followed by β-myrene (7.25%), α-pinene (2.11%), caryophyllene (1.88%), octanal (1.68) and β-phellandrene (1.18%). Some of the minor components included δ-cadinene (0.89%), copaene (0.82%), methyl phthalate (0.54%), linalool (0.48%) and 3-carene (0.21%). The oil extracts exerted different degrees of inhibitory activity against the organisms. The inhibition of the test isolates was dependent on the dissolution solvent used. Methanolic oil mixture inhibited all bacteria and fungi. Ethanol oil mixture inhibited the test bacteria and C. albicans while, the oil extract dissolved in Tween 80 solution showed no inhibitory activity on the test fungi. This study has shown that grape peels from Nigeria contain some antibiotic principles which may be explored for use in the treatment of certain diseases.