Project description:Pancreatic cancer-derived cells NP-18 underwent four rounds of treatment with increasing doses of an adenoviral vector encoding TK enzyme and GCV. Surviving cells were termed NP-18AR and displayed decreased sensitivity to treatment. This experiment analyses the transcriptomic effect of TK/GCV treatment on NP-18AR as compared to that of NP-18 cells. Two-condition experiment, where response to treatment in naïve cells (NP-18) was compared to response to treatment in previously treated resistant cells (NP-18AR). Biological replicates: samples from 3 independently generated and independently treated NP-18AR lines (NP-18AR1, NP-18AR2 and NP-18AR3) were hibridized with 3 independently treated samples of NP-18 cells. A total of 9 hybridizations were performed, 2 for NP-18AR1 (including 1 dye-swap), 4 for NP-18AR2 (including 2 dye swaps) and 3 for NP-18AR3 (including 1 dye-swap).
Project description:Pancreatic cancer-derived cells NP-18 underwent four rounds of treatment with increasing doses of an adenoviral vector encoding TK enzyme and GCV. Surviving cells were termed NP-18AR and displayed decreased sensitivity to treatment. This experiment analyses the transcriptomic effect of TK/GCV treatment on NP-18AR as compared to that of NP-18 cells.
Project description:The combined effects of NP and MBP were much more toxic than NP or MBP exposed alone. We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes and miRNAs after treated with 0.1μM NP, 0.1mM MBP, 0.1μM NP+0.1mM MBP and solvent control.
Project description:To explore the effect of IDO-APT on T cell function, we conducted RNA transcriptome profiling of NPs, named as NP-Scr-APT in article, and NP-IDO-APT treated lymphocytes.
Project description:Objective: Induction of ER stress has been shown to promote NP cell apoptosis and disc degeneration. However, little is known about its regulation by hypoxia and its contribution to extracellular matrix homeostasis. Methods: NP cells were culture under hypoxia (1% O2) and normoxia (21% O2) to assess ER stress status. Tunicamycin and thapsigargin were used to induce canonical ER stress pathways and effects on cell secretome were assessed by proteomic analysis using mass spectrometry. The relevance of these findings to aging and degeneration was investigated by analyzing microarray data of NP tissues from aged mice (GSE134955) and degenerated human discs (GSE70362). Results: NP cells exhibited lower ER stress levels under hypoxia. ER stress inducers tunicamycin and thapsigargin promoted a canonical unfolded protein response. UPR further induced HIF-1 activity under hypoxia. NP cell secretome under ER stress showed an increased secretory pathway with a concomitant decrease in collagens, HAPLN1, and cell adhesion related proteins. Similar to our cell culture studies, NP tissues from aged mice and degenerated human discs presented higher levels of UPR markers and decreased levels of matrix components.