Table 3.
Biological effect/cancer type | Mechanism |
---|---|
• Chronic inflammation and irritation • Deoxyribonucleic acid damages |
• Pro-inflammatory mediators • Progression of malignancies |
• Lead to cancer hallmarks such as CD44, N-cadherin, programmed death ligand 1, and proliferation • Decreased survival rate • Increased the growth of tumours |
• Enhanced the expression level of asialoglycoprotein receptors (ASGR2) |
• Increased cellular oxidative stress | • The toxicological reaction of cancer-coli 2 (Caco-2) cells |
• Inflammation and colon cell permeability are affected • Breast, colon, and liver cancers |
• Elevated levels of interleukin-17 and immunoglobulin A • Induced resistance to conventional chemotherapeutic agents |
• Cause liver and reproductive toxicity • Growth impairments • Breast cancer |
• Overexpressing angiogenesis and nutritional supply • As oestrogen receptor α, the endocrine system mediates human embryonic kidney-oestrogen receptors (HEK-ESR) and human breast cancer cell line (MCF-7) breast cancer cells |
• Breast cancer |
• High protein expression of pituitary tumour-transforming gene 1 (PTTG1) • Increased MCF-7 cell proliferation by suppressing the expression of microRNA (miR-381-3p) |
• Breast cancer • Prostate cancer • Secondary mutagenesis •Tumour development |
• Breaking the deoxyribonucleic acid by double strands causes instability of genomic and chromosome rearrangements |
Various cancer types can be developed due to microplastic exposure, which induces several inflammatory responses and deoxyribonucleic acid damage.
MCF-7 and RNA refer to the human breast cancer cell line and ribonucleic acid, respectively