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

ABSTRACT: 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

ORGANISM(S): Homo sapiens

SUBMITTER: Hee An

PROVIDER: E-GEOD-43598 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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.

2013-01-17 | GSE43598 | GEO

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

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

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

| PRJNA504767 | ENA

Paclitaxel resistance in ovarian cancer increases oncolytic adenovirus efficacy via upregulated CAR expression and dysfunctional cell cycle control

Project description:The microtubule-stabilising drug paclitaxel has activity in relapsed ovarian cancer. However, resistance frequently develops. Oncolytic adenoviruses are a novel cancer therapy, and replicate selectively within and lyse malignant cells, leading to productive infection of neighbouring cells. We found increased efficacy of adenoviruses of multiple subtypes in paclitaxel-resistant ovarian cancer cells. There was increased expression of a key adenovirus receptor, CAR (coxsackie adenovirus receptor), due to increased transcription that resulted from histone modification. Moreover, CAR transcription increased in intraperitoneal xenografts with acquired paclitaxel resistance and in tumours from patients with paclitaxel-resistant ovarian cancer. Finally, we identified dysregulated cell cycle control as a second mechanism of increased adenovirus efficacy in paclitaxel-resistant ovarian cancer and that inhibition of CDK4/6 using PD-0332991 was able both to reverse paclitaxel resistance and reduce adenovirus efficacy. Thus, paclitaxel resistance increases oncolytic adenovirus efficacy via at least two separate mechanisms. Parental SKOV3 and paclitaxel-resistant SKOV3-TR cells were analysed in duplicate

2015-12-10 | E-GEOD-54772 | biostudies-arrayexpress

rhSTIP1 induced SAMD1/5 pathway

Project description:Stress-induced phosphoprotein 1 (STIP1), a co-chaperone that organizes other chaperones- heat shock proteins (HSP), was recently shown to be secreted by human ovarian cancer cells to induce cell proliferation. In neuronal tissues, binding to prion protein was required for STIP1 to activate the ERK (extracellular regulated MAP kinase) signaling pathways. However, in this study, we found that STIP1 stimulated cell proliferation of ovarian cancer via a bone morphogenetic protein (BMP) signaling pathway, not through the prion-ERK pathway. The STIP1 binding to a BMP receptor, ALK2 (activin A receptor, type II-like kinase 2), was necessary and sufficient to stimulate cancer cell proliferation. The binding of STIP1 to ALK2 activated the SMAD signaling pathway, leading to transcriptional activation of ID3 (inhibitor of DNA binding 3) that promotes cell proliferation. In conclusion, ovarian cancer tissues secrete STIP1 into the local environment and eventually into blood circulation of patients. In an autocrine and/or paracrine fashion, secreted STIP1 stimulates cancer cell proliferation by binding to ALK2 and activating the SMAD-ID3 signaling pathways. Elucidation of the mechanism by which STIP1 stimulates cancer cell proliferation may pave the way for developing novel therapeutic strategies for treatment of ovarian cancer. SKOV3 cell,treated without rhSTIP1 SKOV3 cell,treated with rhSTIP1 SKOV3 cell,treated without rhSTIP1-2 SKOV3 cell,treated with rhSTIP1-2

2013-03-09 | E-GEOD-36383 | biostudies-arrayexpress

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

Gene expression deregulation in ovarian cancer cells with acquired inverse resistance to paclitaxel and cisplatin

Project description:Resistance to anti-cancer drugs is the main challenge in oncology. In pre-clinical studies established cancer cell lines are primary tools in deciphering molecular mechanisms of this phenomenon. In this study we proposed a new approach, based on a model of isogenic cancer cell lines with gradually changing resistance. We analyzed trends in gene expression to find out a scaffold of resistance development process. Ovarian cancer cell line A2780 was treated with stepwise increased concentrations of paclitaxel (PTX) to generate a series of drug resistant sublines. To monitor transcriptome changes we submitted them to mRNA-sequencing, followed by identification of differentially expressed genes (DEGs), principal component analysis (PCA) and hierarchical clustering. Functional interactions of proteins, encoded by DEGs, were analyzed by building protein-protein interaction (PPI) networks. We provided a model of human ovarian cancer cell lines with gradually developed resistance to PTX and collateral sensitivity to cisplatin (CDDP) (inverse resistance). In their transcriptomes we identified two groups of DEGs: 1) with fluctuations in expression in the course of resistance acquiring; and 2) with consistently changed expression in each stage of resistance development, constituting a scaffold of the process. In the scaffold PPI network, cell cycle regulator – PLK2; proteins belong to TNF ligand and receptor family as well as ephrin receptor family were found, but proteins linked to osteo- and chondrogenesis and nervous system development turned out to be key players. Our cellular model of drug resistance allowed for keeping track of trends in gene expression and studying this phenomenon as a process of evolution. This approach revealed that abrogation of osteomimic phenotype in ovarian cancer cells may occur during the development of inverse resistance to PTX and CDDP.

2020-12-15 | GSE159791 | GEO

human ovarian cancer cells:parental PTX-sensitive cells (OVCAR-3) vs. PTX-resistant cells (OV3R-PTX)

Project description:Transcriptional profiling (lncRNA and mRNA) of human ovarian cancer cells comparing parental PTX-sensitive cells (OVCAR-3) vs. PTX-resistant cells (OV3R-PTX, derived from OVCAR-3).

2021-03-16 | GSE168927 | GEO

Genetic changes in the evolution of multidrug resistance for cultured human ovarian cancer cells

Project description:Gene expression profiles were assessed for vincristine-sensitive parental ovarian tumor cell line (SKOV3) and its highly vincristine-resistant derivative (SKVCR 2.0) Keywords: vincristine, drug resistance, ovarian, SKOV3, MDR

2007-08-24 | GSE7556 | GEO

ALKBH5 regulates paclitaxel resistance in NSCLC via inhibiting CEMIP-mediated EMT

Project description:N6-methyladenosine (m6A) is the most printed and prevalent mRNA modification, which was verified to be closely correlated with cancer occurrence and progression. As m6A demethlyase, the dysregulation of ALKBH5 was observed in various cancer. However, the role and underlying machinery of ALKBH5 in NSCLC pathogenesis, especially the chemo-resistance was poorly elucidated. The current study indicated that ALKBH5 was decreased during paclitaxel (PTX) resistant process and its down-regulation usually implied poor prognosis of NSCLC patients. Over-expression of ALKBH5 in PTX-resistant cells could suppressed cell proliferation and enhanced chemo-sensitivity. Whereas, knockdown of ALKBH5 exerted opposite effect, which further supported the tumor suppressive role of ALKBH5. Over-expression of ALKBH5 also could reverse the EMT process in PTX-resistant cancer cells. Mechanistically, data of RNA-seq, Real-time PCR and western blotting indicted that CEMIP, also known as KIAA1199, may be the downstream target of ALKBH5. And ALKBH5 could negatively regulated the CEMIP level by decreasing its mRNA stability. Collectively, current data demonstrated that ALKBH5/CEMIP axis modulates the EMT process in NSCLC, which in turn regulates chemo-sensitivity of cancer cells to PTX.

2024-03-12 | GSE243199 | GEO

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