Moreover, xenograft tumors induced by A549/DDP cells exerted cisplatin resistance, and miR-186-5p overexpression could inhibit tumor growth under DDP treatment.
This study aimed to investigate the role of long non-coding RNA (lncRNA) X-inactive specific transcript (XIST) and multidrug resistance-1 (MDR1) in tumor tissue samples and the chemoresistant human NSCLC cell lines, H460/DDP and A549/DDP, and in a murine A549/DDP tumor xenograft.
However, an appropriate length MTS (MethaneThioSulfonate) cross-linking reagent (MTS14) restricted the activation of TREK-1_A286C channels by repeated application of FFA.
In both PT and MTS lower SST2A and CgA expression levels were found in tumors originating from the appendix or colon, compared to tumors from other origins.
The mild PT-CCT treatment completely eradicated MCF-7/ADR and OVCAR-3/DDP tumors without skin damage or tumor recurrence for 30 days, exhibiting synergistic MDR-reversal and superior antitumor efficacy in vivo.
Two new cobalt bis-iminopyridines, [Co(DDP)(H2O)2](NO3)2 (1, DDP = cis-[1,3-bis(2-pyridinylenamine)] cyclohexane) and [Co(cis-DDOP)(NO3)](NO3) (2, cis-DDOP = cis-3,5-bis[(2-Pyridinyleneamin]-trans-hydroxycyclohexane) electrocatalyse the 4-proton, 4-electron reduction of acetonitrile to ethylamine.
The present study observed that in ovarian cancer cells, the expression of ABCG2 was significantly upregulated in response to cis-diamminedichloroplatinum (cisplatin/DDP) treatment, in addition the expression of NOS1 exhibited an increasing trend.
Overall, 412 samples from 165 GEP-NEN patients, comprising both primary tumors (PT) and metastases (MTS), originating from different parts of the gastrointestinal tract or the pancreas were evaluated for SST and CXCR4 expression by means of immunohistochemistry using monoclonal antibodies.
The mild PT-CCT treatment completely eradicated MCF-7/ADR and OVCAR-3/DDP tumors without skin damage or tumor recurrence for 30 days, exhibiting synergistic MDR-reversal and superior antitumor efficacy in vivo.
Two new cobalt bis-iminopyridines, [Co(DDP)(H2O)2](NO3)2 (1, DDP = cis-[1,3-bis(2-pyridinylenamine)] cyclohexane) and [Co(cis-DDOP)(NO3)](NO3) (2, cis-DDOP = cis-3,5-bis[(2-Pyridinyleneamin]-trans-hydroxycyclohexane) electrocatalyse the 4-proton, 4-electron reduction of acetonitrile to ethylamine.
Pathogenic mutations have been identified in the TIMM8A (DDP) and DNAJC19 (TIMM14) genes and are linked to Mohr-Tranebjærg syndrome and dilated cardiomyopathy syndrome (with and without ataxia), respectively.
AE patients had a lower rate of concordant FDG PET (p < 0.05) and required more frequently intracerebral electrodes compared to MTS patients (p < 0.05).
This study aimed to investigate the role of long non-coding RNA (lncRNA) X-inactive specific transcript (XIST) and multidrug resistance-1 (MDR1) in tumor tissue samples and the chemoresistant human NSCLC cell lines, H460/DDP and A549/DDP, and in a murine A549/DDP tumor xenograft.
However, we observe that YTHDF1 high expression correlates with better clinical outcome, with its depletion rendering cancerous cells resistant to cisplatin (DDP) treatment.
This study aimed to investigate the role of long non-coding RNA (lncRNA) X-inactive specific transcript (XIST) and multidrug resistance-1 (MDR1) in tumor tissue samples and the chemoresistant human NSCLC cell lines, H460/DDP and A549/DDP, and in a murine A549/DDP tumor xenograft.
The present study observed that in ovarian cancer cells, the expression of ABCG2 was significantly upregulated in response to cis-diamminedichloroplatinum (cisplatin/DDP) treatment, in addition the expression of NOS1 exhibited an increasing trend.
RESULTS We found that the IC50 value of DDP (Cisplatin) to CHEK2Y390C expressed MDA-MB-231 cells was significantly higher than that of the CHEK2 WT expressed cells and the control cells.
The PMS2 mutation was identified in a 57-year-old woman with a sebaceous adenoma and history of endometrial cancer; to our knowledge, this is the first time a PMS2 mutation has been reported in MTS.
In this study, we found that ectopic miR-181b expression suppressed cancer stem cell properties and enhanced sensitivity to cisplatin (DDP) treatment by directly targeting Notch2. miR-181b could inactivate the Notch2/Hes1 signalling pathway.
In addition, the MVP-mediated downstream effector mTOR2/AKT was disrupted after application of YPFS<sub>+GF</sub> in DDP-treated A549/DDP cell: this disruption was characterized by the decline of mTORC2 components, e.g., Rictor, p-mTOR, as well as the phosphorylation level of its downstream protein AKT.
Compared with the control and negative control groups, the mRNA and protein expressions of PI3K, Akt, mTOR, and bcl-2 decreased, whereas the mRNA and protein expression of bax and the sensitivity of cells to DDP significantly increased.
Our findings demonstrate that Panx-1 is involved in DDP-resistance and ATP/IP<sub>3</sub> pathway mediated by Panx-1 channels participates in DDP-induced apoptosis in testicular cancer.