scholarly journals Cisplatin, glutathione and the third wheel: a copper-(1,10-phenanthroline) complex modulates cisplatin–GSH interactions from antagonism to synergism in cancer cells resistant to cisplatin

RSC Advances ◽  
2019 ◽  
Vol 9 (10) ◽  
pp. 5362-5376 ◽  
Author(s):  
Sarah Vascellari ◽  
Elisa Valletta ◽  
Daniela Perra ◽  
Elisabetta Pinna ◽  
Alessandra Serra ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Cisplatin Resistance ◽  
Drug Cocktail ◽  
The Third ◽  
New Drug ◽  
Early Apoptosis ◽  
Phenanthroline Complex ◽  
Resistant Cells

A new drug cocktail is proposed to overcome the cisplatin-resistance due to the presence of glutathione. A2780 cisplatin-resistant cells, treated with the drug cocktail, showed early apoptosis.

scholarly journals HOTTIP-miR-205-ZEB2 Axis Confers Cisplatin Resistance to Ovarian Cancer Cells

2021 ◽  
Vol 9 ◽  
Author(s):  
Yu-Jie Dong ◽  
Wei Feng ◽  
Yan Li
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Cisplatin Resistance ◽  
Clinical Problem ◽  
Ovarian Cancer Cells ◽  
Stem Cell Markers ◽  
Gene Target ◽  
Gynecological Malignancy ◽  
Clonogenic Potential ◽  
Resistant Cells

Ovarian cancer is a deadly gynecological malignancy with resistance to cisplatin a major clinical problem. We evaluated a role of long non-coding (lnc) RNA HOTTIP (HOXA transcript at the distal tip) in the cisplatin resistance of ovarian cancer cells, using paired cisplatin sensitive and resistant A2780 cells along with the SK-OV-3 cells. HOTTIP was significantly elevated in cisplatin resistant cells and its silencing reversed the cisplatin resistance of resistant cells. HOTTIP was found to sponge miR-205 and therefore HOTTIP silenced cells had higher levels of miR-205. Downregulation of miR-205 could attenuate HOTTIP-silencing effects whereas miR-205 upregulation in resistant cells was found to re-sensitize cells to cisplatin. HOTTIP silencing also led to reduced NF-κB activation, clonogenic potential and the reduced expression of stem cell markers SOX2, OCT4, and NANOG, an effect that could be attenuated by miR-205. Finally, ZEB2 was identified as the gene target of miR-205, thus completing the elucidation of HOTTIP-miR-205-ZEB2 as the novel axis which is functionally involved in the determination of cisplatin resistance in ovarian cancer cells.

LncRNA-SNHG7 interferes with miR-34a to de-sensitize gastric cancer cells to cisplatin

2020 ◽  
pp. 1-11
Author(s):  
Li-Juan Pei ◽  
Peng-Jun Sun ◽  
Kui Ma ◽  
Yan-Yan Guo ◽  
Ling-Yan Wang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cisplatin Resistance ◽  
Luciferase Assay ◽  
Gastric Cancer Cells ◽  
Non Coding Rna ◽  
Important Regulator ◽  
Cancer Tissues ◽  
Long Non Coding Rna ◽  
Resistant Cells

Gastric cancer (GC) remains poor prognosis and survival issues due to the resistance of chemotherapies, such as cisplatin. The long non-coding RNA small nucleolar RNA host gene 7 (lncRNA-SNHG7) is known as an oncogenic molecule in diverse cancers. Here, we demonstrate that SNHG7 was significantly upregulated in gastric cancer and positively correlated with cisplatin resistance of gastric cancer cells that SNHG7 was significantly upregulated in cisplatin resistant cells. Silencing SNHG7 dramatically sensitized cisplatin resistant cells. In contrast, a negative correlation between lncRNA-SNHG7 and miR-34a was found that miR-34a was downregulated in gastric cancer patient tissues and significantly sensitized cisplatin resistant gastric cancer cells. Intriguingly, bioinformatical analysis indicated miR-34a has putative biding site for SNHG7 and such negative association between SNHG7 and miR-34a was verified in gastric cancer tissues. The cisplatin resistant cells displayed increased glycolysis rate and SNHG7 promoted cellular glycolysis rate of gastric cancer cells. Luciferase assay illustrated LDHA, a glycolysis enzyme, was the direct target of miR-34a. Importantly, inhibiting SNHG7 successfully suppressed LDHA expressions and sensitized cisplatin resistant cells and such inhibitory effects could be recovered by further anti-miR-34a. These findings suggest an important regulator mechanism for the SNHG7-mediated cisplatin resistance via miR-34a/LDHA-glycolysis axis.

UBE2L6 is Involved in Cisplatin Resistance by Regulating the Transcription of ABCB6

2020 ◽  
Vol 20 (12) ◽  
pp. 1487-1496 ◽  
Author(s):  
Midori Murakami ◽  
Hiroto Izumi ◽  
Tomoko Kurita ◽  
Chiho Koi ◽  
Yasuo Morimoto ◽  
...  
Keyword(s):  
Gene Expression ◽  
Promoter Activity ◽  
Anticancer Agent ◽  
Cisplatin Resistance ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Molecular Target ◽  
Transcriptional Level ◽  
And Control ◽  
Resistant Cells

Background: Cisplatin is an important anticancer agent in cancer chemotherapy, but when resistant cells appear, treatment becomes difficult, and the prognosis is poor. Objective: In this study, we investigated the gene expression profile in cisplatin sensitive and resistant cells, and identified the genes involved in cisplatin resistance. Methods: Comparison of gene expression profiles revealed that UBE2L6 mRNA is highly expressed in resistant cells. To elucidate whether UBE2L6 is involved in the acquisition of cisplatin resistance, UBE2L6- overexpressing cells established from cisplatin-sensitive cells and UBE2L6-silenced cells developed from cisplatin- resistant cells were generated, and the sensitivity of cisplatin was examined. Results: The sensitivity of the UBE2L6-overexpressing cells did not change compared with the control cells, but the UBE2L6-silenced cells were sensitized to cisplatin. To elucidate the mechanism of UBE2L6 in cisplatin resistance, we compared the gene expression profiles of UBE2L6-silenced cells and control cells and found that the level of ABCB6 mRNA involved in cisplatin resistance was decreased. Moreover, ABCB6 promoter activity was partially suppressed in UBE2L6-silenced cells. Conclusion: These results suggest that cisplatin-resistant cells have upregulated UBE2L6 expression and contribute to cisplatin resistance by regulating ABCB6 expression at the transcriptional level. UBE2L6 might be a molecular target that overcomes cisplatin resistance.

Glycyrrhiza glabra extract and quercetin reverses cisplatin resistance in triple-negative MDA-MB-468 breast cancer cells via inhibition of cytochrome P450 1B1 enzyme

2017 ◽  
Vol 27 (24) ◽  
pp. 5400-5403 ◽  
Author(s):  
Rajni Sharma ◽  
Linda Gatchie ◽  
Ibidapo S. Williams ◽  
Shreyans K. Jain ◽  
Ram A. Vishwakarma ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cytochrome P450 ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Cisplatin Resistance ◽  
Glycyrrhiza Glabra ◽  
Cytochrome P450 1B1

scholarly journals Platinum Complexes in Colorectal Cancer and Other Solid Tumors

Cancers ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 2073
Author(s):  
Beate Köberle ◽  
Sarah Schoch
Keyword(s):  
Colorectal Cancer ◽  
Dna Damage ◽  
Dna Repair ◽  
Cancer Cells ◽  
Cisplatin Resistance ◽  
Platinum Complexes ◽  
Dna Lesions ◽  
Dna Damage Signaling ◽  
Repair Mechanisms ◽  
P53 Inactivation

Cisplatin is one of the most commonly used drugs for the treatment of various solid neoplasms, including testicular, lung, ovarian, head and neck, and bladder cancers. Unfortunately, the therapeutic efficacy of cisplatin against colorectal cancer is poor. Various mechanisms appear to contribute to cisplatin resistance in cancer cells, including reduced drug accumulation, enhanced drug detoxification, modulation of DNA repair mechanisms, and finally alterations in cisplatin DNA damage signaling preventing apoptosis in cancer cells. Regarding colorectal cancer, defects in mismatch repair and altered p53-mediated DNA damage signaling are the main factors controlling the resistance phenotype. In particular, p53 inactivation appears to be associated with chemoresistance and poor prognosis. To overcome resistance in cancers, several strategies can be envisaged. Improved cisplatin analogues, which retain activity in resistant cancer, might be applied. Targeting p53-mediated DNA damage signaling provides another therapeutic strategy to circumvent cisplatin resistance. This review provides an overview on the DNA repair pathways involved in the processing of cisplatin damage and will describe signal transduction from cisplatin DNA lesions, with special attention given to colorectal cancer cells. Furthermore, examples for improved platinum compounds and biochemical modulators of cisplatin DNA damage signaling will be presented in the context of colon cancer therapy.

Novel alkoxyamide-based histone deacetylase inhibitors reverse cisplatin resistance in chemoresistant cancer cells

2020 ◽  
Vol 28 (1) ◽  
pp. 115108 ◽  
Author(s):  
Yodita Asfaha ◽  
Christian Schrenk ◽  
Leandro A. Alves Avelar ◽  
Friedrich Lange ◽  
Chenyin Wang ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Histone Deacetylase ◽  
Histone Deacetylase Inhibitors ◽  
Cisplatin Resistance

scholarly journals Induction of ferroptosis by ATF3 elevation alleviates cisplatin resistance in gastric cancer by restraining Nrf2/Keap1/xCT signaling

2021 ◽  
Vol 26 (1) ◽  
Author(s):  
Dazhi Fu ◽  
Chunxiao Wang ◽  
Lei Yu ◽  
Rui Yu
Keyword(s):  
Cisplatin Resistance ◽  
Activating Transcription Factor 3 ◽  
Advanced Gastric Carcinoma ◽  
Kaplan Meier ◽  
Promising Therapeutic Approach ◽  
Activating Transcription Factor ◽  
Kaplan Meier Plotter ◽  
Frequent Problem ◽  
Atf3 Expression ◽  
Resistant Cells

Abstract Background Currently, resistance against cisplatin (DDP) is a frequent problem for the success of advanced gastric carcinoma (GC) chemotherapy. Here, we sought to investigate the function of activating transcription factor 3 (ATF3) n GC chemoresistance. Methods Expression of ATF3 was determined in GC cell lines (MNK45, SGC7901, and BGC823) and cisplatin (DDP)-resistant cells (SGC7901/DDP and BGC823/DDP). Biological informatics was performed to analyze ATF3 expression and prognosis in GC patients. Cisplatin resistance was evaluated. Ferroptosis was detected after ATF3 transfection of cells. The underlying molecular mechanism was also investigated. Results Transcripts of ATF3 were decreased in GC cells and GC tissues. Kaplan–Meier plotter analysis revealed that ATF3 expression was positively related to the overall survival of GC patients. In particular, lower levels of ATF3 were observed in cisplatin-resistant SGC7901/DDP and BGC823/DDP relative to their parental cells. Notably, ATF3 elevation sensitized cisplatin-resistant cells to cisplatin. Mechanically, compared with parental cells, SGC7901/DDP and BGC823/DDP cells exhibited lower ferroptosis evident by lower ROS, MDA and lipid peroxidation and higher intracellular GSH levels. However, ATF3 elevated ferroptosis in SGC7901/DDP and BGC823/DDP cells. Intriguingly, ATF3 overexpression together with ferroptosis activator erastin or RSL3 treatment further enhanced ferroptosis and cisplatin resistance; however, the ferroptosis suppressor liproxstatin-1 reversed the function of ATF3 in ferroptosis and cisplatin resistance. Additionally, cisplatin-resistant cells exhibited stronger activation of Nrf2/Keap1/xCT signaling relative to parental cells, which was restrained by ATF3 up-regulation. Importantly, restoring Nrf2 signaling overturned ATF3-mediated ferroptosis and cisplatin resistance. Conclusion ATF3 may sensitize GC cells to cisplatin by induction of ferroptosis via blocking Nrf2/Keap1/xCT signaling, supporting a promising therapeutic approach for overcoming chemoresistance in GC.

scholarly journals Bitter Melon (Momordica charantia) Extract Inhibits Tumorigenicity and Overcomes Cisplatin-Resistance in Ovarian Cancer Cells Through Targeting AMPK Signaling Cascade

2016 ◽  
Vol 15 (3) ◽  
pp. 376-389 ◽  
Author(s):  
Mingo M. H. Yung ◽  
Fiona A. Ross ◽  
D. Grahame Hardie ◽  
Thomas H. Y. Leung ◽  
Jinbiao Zhan ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Cisplatin Resistance ◽  
Momordica Charantia ◽  
Signaling Cascade ◽  
Ovarian Cancer Cells ◽  
Bitter Melon ◽  
Ampk Signaling

The third-generation EGFR inhibitor almonertinib (HS-10296) resensitizes ABCB1-overexpressing multidrug-resistant cancer cells to chemotherapeutic drugs

2021 ◽  
pp. 114516
Author(s):  
Chung-Pu Wu ◽  
Tai-Ho Hung ◽  
Sabrina Lusvarghi ◽  
Yi-Hsuan Chu ◽  
Sung-Han Hsiao ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Multidrug Resistant ◽  
Third Generation ◽  
Egfr Inhibitor ◽  
Chemotherapeutic Drugs ◽  
The Third

Practical prescribing

1987 ◽  
Vol 25 (20) ◽  
pp. 80-80
Author(s):  
Martin J Brodie ◽  
Ian Harrison
Keyword(s):  
Side Effects ◽  
Drug Interactions ◽  
Shelf Life ◽  
Text Book ◽  
The Third ◽  
New Drug ◽  
Making Choices ◽  
Treatment Policies ◽  
Accessible Form

This book is a practical manual for the prescriber rather than a text book. The first chapter usefully explains pharmacological terms which are used later in the book. This is followed by three sections concerned with choosing drugs. The first section gives a list of ‘best buys’ for common complaints, the second looks at treatment policies and the third gives basic pharmacological information to help in making choices. Side-effects and drug interactions are presented in the next two chapters in a readily accessible form. The final chapter, called ‘Cautions,’ has some useful information not readily found elsewhere including data on teratogenesis and shelf-life of formulations. It also suggests which drugs we should stop using, and discusses factors to consider before using a new drug.

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