chiniofon and Carcinoma--Non-Small-Cell-Lung

chiniofon has been researched along with Carcinoma--Non-Small-Cell-Lung* in 2 studies

Other Studies

2 other study(ies) available for chiniofon and Carcinoma--Non-Small-Cell-Lung

Article	Year
IOX-101 Reverses Drug Resistance Through Suppression of Akt/mTOR/NF-κB Signaling in Cancer Stem Cell-Like, Sphere-Forming NSCLC Cell. Oncology research, 2020, Mar-27, Volume: 28, Issue:2 Topics: A549 Cells; AC133 Antigen; Apoptosis; ATP Binding Cassette Transporter, Subfamily B; Carcinoma, Non-Small-Cell Lung; Cell Proliferation; Drug Resistance, Neoplasm; Gene Expression Regulation, Neoplastic; Glutathione Transferase; Humans; Hydroxyquinolines; Low Density Lipoprotein Receptor-Related Protein-1; Neoplastic Stem Cells; NF-kappa B; Proto-Oncogene Proteins c-akt; Proto-Oncogene Proteins c-bcl-2; Signal Transduction; Spheroids, Cellular; TOR Serine-Threonine Kinases	2020
E2F inhibition synergizes with paclitaxel in lung cancer cell lines. PloS one, 2014, Volume: 9, Issue:5 The CDK/Rb/E2F pathway is commonly disrupted in lung cancer, and thus, it is predicted that blocking the E2F pathway would have therapeutic potential. To test this hypothesis, we have examined the activity of HLM006474 (a small molecule pan-E2F inhibitor) in lung cancer cell lines as a single agent and in combination with other compounds. HLM006474 reduces the viability of both SCLC and NSCLC lines with a biological IC50 that varies between 15 and 75 µM, but with no significant difference between the groups. Combination of HLM006474 with cisplatin and gemcitabine demonstrate little synergy; however, HLM006474 synergizes with paclitaxel. Surprisingly, we discovered that brief treatment of cells with HLM006474 led to an increase of E2F3 protein levels (due to de-repression of these promoter sites). Since paclitaxel sensitivity has been shown to correlate with E2F3 levels, we hypothesized that HLM006474 synergy with paclitaxel may be mediated by transient induction of E2F3. To test this, H1299 cells were depleted of E2F3a and E2F3b with siRNA and treated with paclitaxel. Assays of proliferation showed that both siRNAs significantly reduced paclitaxel sensitivity, as expected. Taken together, these results suggest that HLM006474 may have efficacy in lung cancer and may be useful in combination with taxanes. Topics: Aminopyridines; Antineoplastic Combined Chemotherapy Protocols; Carcinoma, Non-Small-Cell Lung; Cell Line, Tumor; Cell Proliferation; Cell Survival; Cisplatin; Deoxycytidine; Drug Synergism; E2F3 Transcription Factor; Gemcitabine; Humans; Hydroxyquinolines; Inhibitory Concentration 50; Lung Neoplasms; Paclitaxel; RNA, Small Interfering; Small Cell Lung Carcinoma	2014

Article

Year

IOX-101 Reverses Drug Resistance Through Suppression of Akt/mTOR/NF-κB Signaling in Cancer Stem Cell-Like, Sphere-Forming NSCLC Cell.

Oncology research, 2020, Mar-27, Volume: 28, Issue:2

Topics: A549 Cells; AC133 Antigen; Apoptosis; ATP Binding Cassette Transporter, Subfamily B; Carcinoma, Non-Small-Cell Lung; Cell Proliferation; Drug Resistance, Neoplasm; Gene Expression Regulation, Neoplastic; Glutathione Transferase; Humans; Hydroxyquinolines; Low Density Lipoprotein Receptor-Related Protein-1; Neoplastic Stem Cells; NF-kappa B; Proto-Oncogene Proteins c-akt; Proto-Oncogene Proteins c-bcl-2; Signal Transduction; Spheroids, Cellular; TOR Serine-Threonine Kinases

2020

E2F inhibition synergizes with paclitaxel in lung cancer cell lines.

PloS one, 2014, Volume: 9, Issue:5

The CDK/Rb/E2F pathway is commonly disrupted in lung cancer, and thus, it is predicted that blocking the E2F pathway would have therapeutic potential. To test this hypothesis, we have examined the activity of HLM006474 (a small molecule pan-E2F inhibitor) in lung cancer cell lines as a single agent and in combination with other compounds. HLM006474 reduces the viability of both SCLC and NSCLC lines with a biological IC50 that varies between 15 and 75 µM, but with no significant difference between the groups. Combination of HLM006474 with cisplatin and gemcitabine demonstrate little synergy; however, HLM006474 synergizes with paclitaxel. Surprisingly, we discovered that brief treatment of cells with HLM006474 led to an increase of E2F3 protein levels (due to de-repression of these promoter sites). Since paclitaxel sensitivity has been shown to correlate with E2F3 levels, we hypothesized that HLM006474 synergy with paclitaxel may be mediated by transient induction of E2F3. To test this, H1299 cells were depleted of E2F3a and E2F3b with siRNA and treated with paclitaxel. Assays of proliferation showed that both siRNAs significantly reduced paclitaxel sensitivity, as expected. Taken together, these results suggest that HLM006474 may have efficacy in lung cancer and may be useful in combination with taxanes.

Topics: Aminopyridines; Antineoplastic Combined Chemotherapy Protocols; Carcinoma, Non-Small-Cell Lung; Cell Line, Tumor; Cell Proliferation; Cell Survival; Cisplatin; Deoxycytidine; Drug Synergism; E2F3 Transcription Factor; Gemcitabine; Humans; Hydroxyquinolines; Inhibitory Concentration 50; Lung Neoplasms; Paclitaxel; RNA, Small Interfering; Small Cell Lung Carcinoma

2014