Table 2.
Involvement of beta-END in cancer.
| Tumor | Beta-Endorphin | References |
|---|---|---|
| Bone | Cinobufagin promoted beta-END mRNA and protein expressions in microglia. It upregulated the expressions of mu-opioid receptors and beta-END in the tumor and tissues placed close to the tumor. | [130,131] |
| Brain | Beta-END-binding sites in human glioblastoma cells. Beta-END in human brain tumor cyst fluids. |
[140,141] |
| Breast | High plasma beta-END levels in healthy women were even higher in healthy postmenopausal women; lower in women with breast cancer. Chemotherapy improved beta-END levels in postmenopausal women. END did not affect the migratory capacity of human breast carcinoma cells. Beta-END expression in cells and stroma of human breast cancer samples. Beta-END activates survival/mitogenic signaling pathways in human cancer cells. Increasing plasma beta-END levels correlated with increasing tumor burden. A correlation between increased plasma beta-END levels and improved quality of life in breast cancer patients. Beta-END counteracts breast cancer development by favoring immune-mediated anticancer defenses. Beta-END alters the tumor microenvironment. |
[144,145,149,151,155,156,157,177] |
| Cervical | Electroacupuncture increases plasma beta-END levels in humans. | [160] |
| Colorectal | Beta-END in adenocarcinomas derived from the colon mucosa; its expression is higher in adenocarcinomas than in the mucosal layer of normal colons. Beta-END in rectal carcinoids. Beta-END did not affect tumor cell migration, viability, chemotaxis, or invasion. Colon carcinoma symptoms decreased after ultraviolet A eye irradiation; these effects were reduced when beta-END inhibitors were administered and totally disappeared with naltrexone. Animals with hypothalamic beta-END neuronal transplants failed to develop tumors and showed a lesser adenoma development. Beta-END administration into the raphe magnus nucleus: favored metastasis inhibited with naloxone, and when this nucleus was electrically stimulated, metastasis was attenuated. |
[162,167,168,169,170,172,186] |
| Gastric | Beta-END in adenocarcinomas derived from the antral mucosa. Plasma beta-END level decreased in patients after transcutaneous electrical stimulation. |
[177,178] |
| Head and neck | Beta-END did not affect the migration, chemotaxis, or invasion of squamous carcinoma cells. Beta-END did not affect either the differentiation or the viability of tumor cells. Beta-END increased the production of leukocyte migration inhibitory factor, reaching almost normal levels in patients with squamous carcinoma. |
[172,185,186,187] |
| Larynx | Beta-END in tumor cells. | [189] |
| Leukemia | Beta-END in the cerebrospinal fluid of children with acute lymphoblastic leukemia: highest levels observed at the end of the intensification chemotherapy; glucocorticoid treatment decreased beta-END levels. Plasma beta-END levels decreased in patients with solid tumors after treatment with a chemotherapeutic drug. Plasma beta-END levels are higher in patients with acute leukemia than in healthy individuals. Beta-END promoted the growth of T-lymphoblastoid cells. |
[194,195,196,197] |
| Liver | Neurons expressing beta-END transplanted into the hypothalamus prevented hepatocellular carcinoma formation. This strategy inhibited carcinogen-induced liver histopathologies and augmented the concentration of NK cell cytotoxic agents. |
[201] |
| Lung | Beta-END in the bronchoalveolar lavage fluid/plasma of patients. Beta-END in lung small-cell carcinomas and carcinoid tumors. U1,690 cell line expresses beta-END, and the peptide promotes its proliferation through non-opioid binding sites. Beta-END acts as a chemoattractant for small-cell lung carcinoma cells favoring migration and metastasis. |
[210,211,212,214,215] |
| Melanoma | Beta-END in human samples. Beta-END in secondary neuroendocrine carcinomas of the skin but not in primary carcinomas. B16 melanoma cells synthesize and release beta-END. B16 cells decreased tumor growth in mu-opioid receptor-deficient animals. A correlation occurs between beta-END levels and tumor progression. Beta-END immunoreactivity: lower in benign melanocytic naevi than in metastatic and advanced melanomas. |
[221,232,233] |
| Neuroblastoma | Beta-END-binding sites expression. MET decreased the tumor mitotic index, which was counteracted with naltrexone. |
[238,239] |
| Ovarian | Beta-END in ovarian sex cord-stromal tumors and ovarian carcinoids. A positive correlation between patients’ survival time/disease-free time and plasma beta-END levels. Lower beta-END concentrations were observed in patients with recurrence Beta-END blocked the proliferation of human ovarian KF cancer cells; this effect was counteracted with naloxone. |
[244,247,248,249] |
| Pancreatic | Beta-END did not affect tumor cell migration, chemotaxis, or invasion (MIA PaCa-2, PANC-1, BxPC-3). | [186] |
| Pheochromocytoma | Beta-END expression and release. | [257,259,260] |
| Pituitary | Beta-END in pituitary adenomas. Beta-END released from human cancer cells. Beta-END presence in clinically silent pituitary corticotroph adenomas. Beta-END/beta-END1-27 in extracts of pituitary melanotroph tumors transplanted subcutaneously. W7 potentiated the release of beta-END from cancer cells. |
[266,267,268,269,270] |
| Prostate | Beta-END in prostatic carcinomas. Rats with transplanted neurons expressing beta-END into the hypothalamic paraventricular nucleus showed a protective effect against prostate cancer development. |
[275,276] |
| Retinoblastoma | Beta-END-binding sites in human cell lines. | [283] |
| Thymic | Beta-END binds to non-opioid binding sites expressed in thymoma cells. Beta-END in an oncocytic carcinoid tumor of the thymus. |
[286,287] |
| Thyroid | Presence of opioid peptides derived from the three opioid precursors in human thyroid medullary carcinomas. Beta-END released from cultured medullary thyroid carcinoma cells. |
[11,290] |