pd-168368 and Breast-Neoplasms

pd-168368 has been researched along with Breast-Neoplasms* in 2 studies

Other Studies

2 other study(ies) available for pd-168368 and Breast-Neoplasms

Article	Year
Neuromedin B receptor antagonism inhibits migration, invasion, and epithelial-mesenchymal transition of breast cancer cells. International journal of oncology, 2016, Volume: 49, Issue:3 Neuromedin B (NMB) acts as an autocrine growth factor and a pro-angiogenic factor. Its receptor, NMB receptor (NMB-R), is overexpressed in solid tumors. In the present study, we showed that an NMB-R antagonist, PD168368, suppresses migration and invasion of the human breast cancer cell line MDA-MB-231. In addition, PD168368 reduced epithelial-mesenchymal transition (EMT) of breast cancer cells by E-cadherin upregulation and vimentin downregulation. Moreover, we found that PD168368 potently inhibits in vivo metastasis of breast cancer. Taken together, these findings suggest that NMB-R antagonism may be an alternative approach to prevent breast cancer metastasis, and targeting NMB-R may provide a novel therapeutic strategy for breast cancer treatment. Topics: Animals; Antineoplastic Agents; Breast Neoplasms; Cadherins; Cell Line, Tumor; Cell Movement; Epithelial-Mesenchymal Transition; Female; Humans; Indoles; MCF-7 Cells; Mice; Neoplasm Invasiveness; Neoplasm Metastasis; Pyridines; Vimentin; Xenograft Model Antitumor Assays	2016
Neuromedin B receptor antagonist suppresses tumor angiogenesis and tumor growth in vitro and in vivo. Cancer letters, 2011, Dec-15, Volume: 312, Issue:1 Neuromedin B (NMB), a member of the mammalian bombesin-like peptide family, and its receptor were aberrantly expressed in vascularized solid tumors. Here, the NMB receptor (NMB-R) antagonist PD168368 specifically inhibited both NMB-induced in vivo and in vitro angiogenesis. In addition, PD168368 showed growth inhibitory effects on MDA-MB-231 breast cancer cells by inducing cell cycle arrest and apoptosis. Furthermore, PD168368 effectively suppressed tumor growth in a xenograft model of breast tumor in vivo. Overall, NMB-R antagonist exhibited a significant antitumor activity by simultaneously inhibiting neovascularization and cancer cell growth, thereby suggesting that NMB-R could be a potential therapeutic target for cancer treatment. Topics: Animals; Breast Neoplasms; Cell Growth Processes; Female; Humans; Indoles; Male; Mice; Mice, Inbred C57BL; Mice, Nude; Neovascularization, Pathologic; Pyridines; Rats; Rats, Sprague-Dawley; Receptors, Bombesin; Xenograft Model Antitumor Assays	2011

Article

Year

Neuromedin B receptor antagonism inhibits migration, invasion, and epithelial-mesenchymal transition of breast cancer cells.

International journal of oncology, 2016, Volume: 49, Issue:3

Neuromedin B (NMB) acts as an autocrine growth factor and a pro-angiogenic factor. Its receptor, NMB receptor (NMB-R), is overexpressed in solid tumors. In the present study, we showed that an NMB-R antagonist, PD168368, suppresses migration and invasion of the human breast cancer cell line MDA-MB-231. In addition, PD168368 reduced epithelial-mesenchymal transition (EMT) of breast cancer cells by E-cadherin upregulation and vimentin downregulation. Moreover, we found that PD168368 potently inhibits in vivo metastasis of breast cancer. Taken together, these findings suggest that NMB-R antagonism may be an alternative approach to prevent breast cancer metastasis, and targeting NMB-R may provide a novel therapeutic strategy for breast cancer treatment.

Topics: Animals; Antineoplastic Agents; Breast Neoplasms; Cadherins; Cell Line, Tumor; Cell Movement; Epithelial-Mesenchymal Transition; Female; Humans; Indoles; MCF-7 Cells; Mice; Neoplasm Invasiveness; Neoplasm Metastasis; Pyridines; Vimentin; Xenograft Model Antitumor Assays

2016

Neuromedin B receptor antagonist suppresses tumor angiogenesis and tumor growth in vitro and in vivo.

Cancer letters, 2011, Dec-15, Volume: 312, Issue:1

Neuromedin B (NMB), a member of the mammalian bombesin-like peptide family, and its receptor were aberrantly expressed in vascularized solid tumors. Here, the NMB receptor (NMB-R) antagonist PD168368 specifically inhibited both NMB-induced in vivo and in vitro angiogenesis. In addition, PD168368 showed growth inhibitory effects on MDA-MB-231 breast cancer cells by inducing cell cycle arrest and apoptosis. Furthermore, PD168368 effectively suppressed tumor growth in a xenograft model of breast tumor in vivo. Overall, NMB-R antagonist exhibited a significant antitumor activity by simultaneously inhibiting neovascularization and cancer cell growth, thereby suggesting that NMB-R could be a potential therapeutic target for cancer treatment.

Topics: Animals; Breast Neoplasms; Cell Growth Processes; Female; Humans; Indoles; Male; Mice; Mice, Inbred C57BL; Mice, Nude; Neovascularization, Pathologic; Pyridines; Rats; Rats, Sprague-Dawley; Receptors, Bombesin; Xenograft Model Antitumor Assays

2011