AI Article Synopsis
- The incidence of colorectal cancer (CRC) is on the rise worldwide, and traditional chemotherapy has significant side effects.
- Low-dose naltrexone (LDN) appears to inhibit CRC progression by increasing M1 macrophage activity and promoting tumor cell apoptosis through specific signaling pathways.
- The study suggests that LDN could be a promising treatment for CRC by reducing tumor size and enhancing immune response, warranting further investigation.
Article Abstract
The incidence of colorectal cancer (CRC) is increasing annually worldwide. However, traditional chemotherapy has obvious side effects. Low-dose naltrexone (LDN) has been reported to delay tumor progression, but the mechanism remains unclear. Therefore, the aim of this study was to explore the mechanisms underlying the inhibitory effect of LDN on CRC progression in vivo and in vitro. We found that expression of macrophage markers (F4/80, CD68) was increased in nude mice treated with LDN compared with the control group (p < 0.05). Additionally, levels of M1 macrophage phenotypic markers (CD80) and cytokines (tumor necrosis factor-α, TNF-α) were higher than in the control group (p < 0.05). LDN was able to upregulate expression of the opioid growth factor receptor (OGFr) and apoptosis-related factors Bax, caspase-9, caspase-3, and PARP and downregulate expression of Bcl-2, Survivin, and Ki67 to promote tumor cell apoptosis. Therefore, we speculate that LDN reduces tumor size by increasing levels of M1-like macrophages and activating the Bax/Bcl-2/caspase-3/PARP signaling pathway to induce apoptosis. We suggest that LDN has potential for the treatment of CRC.
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| http://dx.doi.org/10.1016/j.intimp.2020.106388 | DOI Listing |
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