pm-01183 and Uterine-Cervical-Neoplasms

pm-01183 has been researched along with Uterine-Cervical-Neoplasms* in 2 studies

Other Studies

2 other study(ies) available for pm-01183 and Uterine-Cervical-Neoplasms

Article	Year
Lurbinectedin (PM01183), a selective inhibitor of active transcription, effectively eliminates both cancer cells and cancer stem cells in preclinical models of uterine cervical cancer. Investigational new drugs, 2019, Volume: 37, Issue:5 Objective The objective of this study was to evaluate the antitumor effects of lurbinectedin on cervical cancer with a special focus on its effects on cancer stem cells (CSCs). Methods Using two cervical cell lines (ME180 and CaSki cells), the antitumor effects of lurbinectedin were assessed in vitro using the MTS assay and colony formation assay. The growth inhibitory effects of paclitaxel and cisplatin were also evaluated as controls. By employing ALDH1 activity as a marker of CSCs, the antitumor effects of lurbinectedin on cervical CSCs and non-CSCs were individually evaluated. Finally, we investigated the mechanisms by which lurbinectedin eliminated cervical CSCs. Results Lurbinectedin had significant antitumor activity toward cervical cancer cells at low nanomolar concentrations in vitro. Mouse xenografts of cervical cancer revealed that lurbinectedin significantly inhibits tumor growth. The growth-inhibitory effect of lurbinectedin was greater than that of cisplatin and paclitaxel. ALDH-high CSCs were observed in both cervical cancer cell lines (4.4% and 2.4% in ME180 and CaSki cells, respectively). Lurbinectedin downregulated stem cell-related gene expression (Oct4, Nanog, and SOX2), inhibited HDAC1 activity, and effectively eliminated ALDH-high CSCs. Conclusions Lurbinectedin is highly effective on uterine cervical cancer because it eliminates CSCs, and lurbinectedin is a promising agent to overcome platinum resistance in cervical cancer. Topics: Animals; Antineoplastic Agents; Apoptosis; Carbolines; Cell Proliferation; Cisplatin; Drug Resistance, Neoplasm; Female; Heterocyclic Compounds, 4 or More Rings; Humans; Mice; Mice, Nude; Neoplastic Stem Cells; Tumor Cells, Cultured; Uterine Cervical Neoplasms; Xenograft Model Antitumor Assays	2019
PM01183 inhibits myeloid-derived suppressor cells in vitro and in vivo. Immunotherapy, 2017, Volume: 9, Issue:10 To evaluate the ability of PM01183 to eliminate myeloid-derived suppressor cells (MDSCs).. The effect of PM01183 on MDSCs, NK cells and CD8. PM01183 reduced the number of MDSCs by inducing apoptosis and attenuated the MDSC-mediated suppression of CD8. PM01183 exhibits strong inhibitory effects on MDSCs. Topics: Animals; Antineoplastic Agents; Apoptosis; Arginase; Carbolines; CD8-Positive T-Lymphocytes; Cell Line, Tumor; Female; Heterocyclic Compounds, 4 or More Rings; Humans; Immunosuppression Therapy; Killer Cells, Natural; Lymphocyte Activation; Mice, Inbred BALB C; Mice, Nude; Myeloid-Derived Suppressor Cells; Phosphorylation; STAT3 Transcription Factor; Uterine Cervical Neoplasms	2017

Article

Year

Lurbinectedin (PM01183), a selective inhibitor of active transcription, effectively eliminates both cancer cells and cancer stem cells in preclinical models of uterine cervical cancer.

Investigational new drugs, 2019, Volume: 37, Issue:5

Objective The objective of this study was to evaluate the antitumor effects of lurbinectedin on cervical cancer with a special focus on its effects on cancer stem cells (CSCs). Methods Using two cervical cell lines (ME180 and CaSki cells), the antitumor effects of lurbinectedin were assessed in vitro using the MTS assay and colony formation assay. The growth inhibitory effects of paclitaxel and cisplatin were also evaluated as controls. By employing ALDH1 activity as a marker of CSCs, the antitumor effects of lurbinectedin on cervical CSCs and non-CSCs were individually evaluated. Finally, we investigated the mechanisms by which lurbinectedin eliminated cervical CSCs. Results Lurbinectedin had significant antitumor activity toward cervical cancer cells at low nanomolar concentrations in vitro. Mouse xenografts of cervical cancer revealed that lurbinectedin significantly inhibits tumor growth. The growth-inhibitory effect of lurbinectedin was greater than that of cisplatin and paclitaxel. ALDH-high CSCs were observed in both cervical cancer cell lines (4.4% and 2.4% in ME180 and CaSki cells, respectively). Lurbinectedin downregulated stem cell-related gene expression (Oct4, Nanog, and SOX2), inhibited HDAC1 activity, and effectively eliminated ALDH-high CSCs. Conclusions Lurbinectedin is highly effective on uterine cervical cancer because it eliminates CSCs, and lurbinectedin is a promising agent to overcome platinum resistance in cervical cancer.

Topics: Animals; Antineoplastic Agents; Apoptosis; Carbolines; Cell Proliferation; Cisplatin; Drug Resistance, Neoplasm; Female; Heterocyclic Compounds, 4 or More Rings; Humans; Mice; Mice, Nude; Neoplastic Stem Cells; Tumor Cells, Cultured; Uterine Cervical Neoplasms; Xenograft Model Antitumor Assays

2019

PM01183 inhibits myeloid-derived suppressor cells in vitro and in vivo.

Immunotherapy, 2017, Volume: 9, Issue:10

To evaluate the ability of PM01183 to eliminate myeloid-derived suppressor cells (MDSCs).. The effect of PM01183 on MDSCs, NK cells and CD8. PM01183 reduced the number of MDSCs by inducing apoptosis and attenuated the MDSC-mediated suppression of CD8. PM01183 exhibits strong inhibitory effects on MDSCs.

Topics: Animals; Antineoplastic Agents; Apoptosis; Arginase; Carbolines; CD8-Positive T-Lymphocytes; Cell Line, Tumor; Female; Heterocyclic Compounds, 4 or More Rings; Humans; Immunosuppression Therapy; Killer Cells, Natural; Lymphocyte Activation; Mice, Inbred BALB C; Mice, Nude; Myeloid-Derived Suppressor Cells; Phosphorylation; STAT3 Transcription Factor; Uterine Cervical Neoplasms

2017