Abstract
BackgroundCancer pain is a debilitating disorder of human breast cancer and a primary determinant of the poor quality of life, and relieving pain is fundamental strategy in the cancer treatment. However, opioid analgesics, like morphine and fentanyl, which are widely used in cancer pain treatment have been reported to enhance stem-like traits and epithelial-mesenchymal transition (EMT) of breast cancer cells. As such, it is vital to make the best choice of analgesic for breast cancer management.MethodsMTT assays and colony formation assays were performed to examine tumor cell proliferation upon nalbuphine treatment. RT-PCR, western blot, flow cytometry, sphere formation, immunohistochemistry, transwell assays, wound healing assays and mouse xenograft were used to assess the biological effects of nalbuphine treatment.ResultsNalbuphine inhibited breast cancer cell growth and tumorigenesis, with little effect on noncancerous breast cell lines. Nalbuphine suppressed cancer stem-like traits and EMT in both breast cancer cells and mouse xenograft tumor tissues. Additionally, activation of AKT reversed the nalbuphine-induced inhibition of cancer stem-like properties, tumorigenesis and EMT.ConclusionsOur results demonstrate a new role of nalbuphine in inhibiting cancer stem-like properties and EMT in addition to relieving pain, which suggests that nalbuphine may be effective in breast cancer treatment.
Highlights
Cancer pain is a debilitating disorder of human breast cancer and a primary determinant of the poor quality of life, and relieving pain is fundamental strategy in the cancer treatment
We found that nalbuphine caused a significant dose- and time-dependent decrease in breast cancer cell viability compared with PBS controls (0 μM) (Fig. 1a, b and Additional file 2: Figure S1A)
The 50% inhibitory concentration (IC50) in MDA-MB-231, MCF-7 and SK-BR-3 is listed in Additional file 7: Table S7
Summary
Cancer pain is a debilitating disorder of human breast cancer and a primary determinant of the poor quality of life, and relieving pain is fundamental strategy in the cancer treatment. Opioid analgesics, like morphine and fentanyl, which are widely used in cancer pain treatment have been reported to enhance stem-like traits and epithelial-mesenchymal transition (EMT) of breast cancer cells. A large number of breast cancer patients suffer from cancer-related pains caused by surgery, tumor progression and bone metastasis [1] This leads to the patients’ constant demand for analgesic treatment during breast cancer therapy. Our previous work showed that morphine and fentanyl, the classic opioid analgesics, promoted breast cancer stem-like traits and epithelialmesenchymal transition (EMT) [2, 3]. Our previous results demonstrated that morphine and fentanyl could promote the development of breast cancer cells with stem-like phenotypes [2, 3], but little is known about the effect of nalbuphine on cancer stem-like properties. The effects of nalbuphine on the AKT-NFκB signaling pathway, and further influences on stem-like properties and EMT in breast cancer have not been investigated
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