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BCLIN25 / miRNA-125b axis regulates chemotherapeutic resistance and epithelial-mesenchymal transition

ABSTRACT: paclitaxel-resistant triple-negative breast cancer cell lines (MDA-MB-231/PTX）transfect BCLIN25-specific si-BCLIN25 to knockdown BCLIN25 and analysis differential paclitaxel-resistantlung adenocarcinoma cell lines（PC9/GR）transfect HUMT-specific shHUMT to knockdown HUMT1 and analysis differential

ORGANISM(S): Homo sapiens

PROVIDER: GSE179144 | GEO | 2021/07/06

REPOSITORIES: GEO

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Targeting lncRNA HUMT attenuates chemoresistance of LUAD via impairing glycolysis signaling

Project description:gefitinib-resistant lung adenocarcinoma cell lines（PC9/GR）transfect HUMT-specific shHUMT to knockdown HUMT1 and analysis differential gefitinib-resistant lung adenocarcinoma cell lines（PC9/GR）transfect HUMT-specific shHUMT to knockdown HUMT1 and analysis differential

2021-07-06 | GSE179146 | GEO

The long noncoding RNA SNHG1 promotes carboplatin resistance retinoblastoma

Project description:carboplatin resistance retinoblastoma cell lines (Weri-RB1/CRP) transfect SNHG1-specific shSNHG1 to knockdown SNHG1 and analysis differential gene in Weri-RB1/CRP

2021-04-10 | GSE171455 | GEO

miR-1061 and miR-591 are involved in paclitaxel-resistance and their regulation increases the sensitivity to paclitaxel

Project description:MicroRNA expression in paclitaxel (PTX)-resistant SKpac sublines was compared to that of the PTX-sensitive, parental SKOV3 ovarian cancer cell line using microarray and real-time RT-PCR. The function of differentially expressed microRNAs in chemoresistant ovarian cancer was further evaluated by apoptosis, cell proliferation, and migration assays. Total RNA obtained from four different chemo-resistant subcell lines (skp 41,43,44,46) compared to parent cell line (skov3), human ovary cacinoma

2013-01-17 | E-GEOD-43598 | biostudies-arrayexpress

Transcriptional screening in MDA-231 cells treated with low-dose Paclitaxel for 24 and 48 hours

Project description:Paclitaxel is the most commonly used chemotherapeutic agent in breast cancer treatment. Notably, a comprehensive understanding of paclitaxelâs effects requires insight into the dose-specific activities of paclitaxel and their influence on the cancer cells and host microenvironment. The aim of our study is to reveal the gene transcriptional changes in response to low-Paclitaxel (PTX) treatment in breast cancer cells. For genome-wide gene expression analysis, MDA-MB-231 cells (high-invasive breast cancer cell line) were treated with 5 ng/ml PTX for 24 and 48 hours respectively and then the cell lysates were prepared by TRIzol reagent. Then the total RNA in each group was extracted and the genome-wide gene expressing profile was detected through the Human One Array (HOA) Microarray system (Phalanx Biotech Group, Taiwan).

2016-06-01 | E-GEOD-82048 | biostudies-arrayexpress

miR-1061 and miR-591 are involved in paclitaxel-resistance and their regulation increases the sensitivity to paclitaxel

2013-01-17 | GSE43598 | GEO

IL-8 Confers Acquired Resistance to EGFR Inhibitors through Regulating Stem Cell-like Properties in Lung Cancer

Project description:Previous study has demonstrated that PC9/gef cells are resistant to gefitinib-induced aspoptosis. To investigate the regulators contributed to gefitinib resistance in lung cancer, we analyzed the gene expression profiles between PC9 and PC9/gef cells. Our results showed that IL-8 contributes to gefitinib resistance and cancer stemness. In contrast, IL-8 knockdown decreased stem-like characteristics and increased gefitinib-induced apoptosis in PC9/gef cells. RNAs extracted from gefitinib-sensitive PC9 cells and gefitinib-resistant PC9/gef cells were hybridized on Affymetrix microarrays. We tried to compare the differential gene expression profiles between PC9 and PC9/gef cells to identify the possible regulators in gefitinib resistance.

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KFTX paclitaxel (PTX)-resistant ovarian cancer cells, KFTXlow PTX-resistant ovarian cancer cells and KFlow PTX-sensitive ovarian cancer cells expression profilies

Project description:Oncolytic vaccinia virus (OVV) has demonstrated appropriate safety profiles for clinical development. Although OVV was designed to kill cancer cells efficiently, sensitivity to OVV varies in individual cancers. Here, we found that OVV was much more efficient in KFTX paclitaxel (PTX)-resistant ovarian cancer cells, compared to that in KFlow PTX-sensitive cells. Microarray analysis showed that urothelial carcinoma-associated 1 (UCA1) upregulation contributed to both enhanced PTX resistance and OVV spread.

2018-11-10 | GSE122358 | GEO

Transcriptional screening in MDA-231 cells treated with low-dose Paclitaxel for 24 and 48 hours

Project description:Paclitaxel is the most commonly used chemotherapeutic agent in breast cancer treatment. Notably, a comprehensive understanding of paclitaxel’s effects requires insight into the dose-specific activities of paclitaxel and their influence on the cancer cells and host microenvironment. The aim of our study is to reveal the gene transcriptional changes in response to low-Paclitaxel (PTX) treatment in breast cancer cells.

2016-06-01 | GSE82048 | GEO

Effects of Dihydrotanshinone I on proliferation and invasiveness of Paclitaxel-resistant anaplastic thyroid cancer cells

Project description:ATC is a very rare, but extremely aggressive form of thyroid malignancy, responsible for the highest mortality rate registered for thyroid cancer. In the patients without known genetic aberrations, the current treatment is still represented by palliative surgery and systemic mono- or combined-chemotherapy, which is often not fully effective for appearance of drug resistance. Comprehension of the mechanisms involved in the development of the resistance is therefore an urgent issue to suggest novel therapeutic approaches of this very aggressive malignancy. In this study, we created a model of anaplastic thyroid cancer (ATC) cells resistant to paclitaxel, to investigate the characteristics of these cells by analyzing the profile of gene expression and comparing with that of paclitaxel-sensitive original ATC cell lines. In addition, we evaluated the effects of Dihydrotanshinone I (DHT) on the viability and invasiveness of paclitaxel-resistant cells. ATC paclitaxel-resistant cells highlighted an overexpression of ABCB1 and a hyper-activation of the NF-κB compared to sensitive cells. DHT treatment results in a reduction of cell viability, and clonogenic ability of resistant cells. Moreover, DHT induces a decrement of NF-κB activity in SW1736-PTX and 8505C-PTX cells. In conclusion, to the best of our knowledge, the results of the present study are the first to demonstrate the antitumor effects of DHT on ATC cells resistant to Paclitaxel in vitro.

2021-07-10 | GSE179786 | GEO

Alleviating iatrogenic effects of paclitaxel-coated balloons via anti-inflammatory treatment

Project description:Background: Paclitaxel is touted as an essential medicine due to its extensive use as a chemotherapeutic for various cancers and an antiproliferative agent for restenosis. Due to recent concerns related to long-term mortality, paclitaxel (PTX)-based endovascular therapy is now surrounded by controversies. Objective: Examine the inflammatory mediators driven by the systemic administration of PTX and explore the means to suppress these effects. Methods: RNAseq analysis, cell and mouse models. Results: RNAseq analysis of primary human endothelial cells (ECs) treated with PTX demonstrated transcriptional perturbations of a set of pro-inflammatory mediators, including monocyte chemoattractant protein-1 (MCP-1) and CD137, which were validated in EC lysates. These perturbations were abrogated with dexamethasone, a prototypic anti-inflammatory compound. The media of ECs pre-treated with PTX showed a significant increase in MCP-1 levels, which were reverted to baseline levels with DEX treatment. A group of mice harvested at different time points after PTX injection were analyzed for immediate and delayed effects of PTX. A 3-fold increase in MCP-1 was noted in blood and aortic ECs after 12 hours of PTX treatment. Similar changes in CD137 and downstream mediators such as tissue factor, VCAM-1 and E-selectin were noted in aortic ECs. Conclusions: Our study shows that systemic PTX exposure upregulates atherothrombotic markers, and co-delivery of DEX can subdue the untoward toxic effects. Long-term studies are needed to probe the mechanisms driving systemic complications of PTX-based therapies and evaluate the clinical potential of DEX to mitigate risk.

2023-03-02 | GSE217550 | GEO

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