scholarly journals Arene Ruthenium(II) Complexes Bearing the κ-P or κ-P,κ-S Ph2P(CH2)3SPh Ligand

Molecules ◽  
2021 ◽  
Vol 26 (7) ◽  
pp. 1860
Author(s):  
Sören Arlt ◽  
Vladana Petković ◽  
Gerd Ludwig ◽  
Thomas Eichhorn ◽  
Heinrich Lang ◽  
...  
Keyword(s):  
Resistant Cell ◽  
Sw480 Cell ◽  
Resistant Cell Line ◽  
31P Nmr Spectroscopy ◽  
X Ray Diffraction ◽  
The Stability ◽  
Induced Apoptosis ◽  
13C And 31P Nmr ◽  
Micromolar Range ◽  
Mcf 7

Neutral [Ru(η6-arene)Cl2{Ph2P(CH2)3SPh-κP}] (arene = benzene, indane, 1,2,3,4-tetrahydronaphthalene: 2a, 2c and 2d) and cationic [Ru(η6-arene)Cl(Ph2P(CH2)3SPh-κP,κS)]X complexes (arene = mesitylene, 1,4-dihydronaphthalene; X = Cl: 3b, 3e; arene = benzene, mesitylene, indane, 1,2,3,4-tetrahydronaphthalene, and 1,4-dihydronaphthalene; X = PF6: 4a–4e) complexes were prepared and characterized by elemental analysis, IR, 1H, 13C and 31P NMR spectroscopy and also by single-crystal X-ray diffraction analyses. The stability of the complexes has been investigated in DMSO. Complexes have been assessed for their cytotoxic activity against 518A2, 8505C, A253, MCF-7 and SW480 cell lines. Generally, complexes exhibited activity in the lower micromolar range; moreover, they are found to be more active than cisplatin. For the most active ruthenium(II) complex, 4b, bearing mesitylene as ligand, the mechanism of action against 8505C cisplatin resistant cell line was determined. Complex 4b induced apoptosis accompanied by caspase activation.

IK1 channel activity contributes to cisplatin sensitivity of human epidermoid cancer cells

2008 ◽  
Vol 294 (6) ◽  
pp. C1398-C1406 ◽  
Author(s):  
Elbert L. Lee ◽  
Yuichi Hasegawa ◽  
Takahiro Shimizu ◽  
Yasunobu Okada
Keyword(s):  
Cancer Cells ◽  
Cellular Response ◽  
Physiological Role ◽  
Resistant Cell ◽  
Resistant Cell Line ◽  
Dominant Negative ◽  
Cation Channels ◽  
Channel Activity ◽  
Kb Cells ◽  
Induced Apoptosis

Cisplatin, a platinum-based drug, is an important weapon against many types of cancer. It induces apoptosis by forming adducts with DNA, although many aspects of its mechanism of action remain to be clarified. Previously, we found a role for the volume-sensitive, outwardly rectifying Cl− channel in cisplatin-induced apoptosis. To investigate the possibility that cation channels also have a role in the cellular response to cisplatin, we examined the activity of cation channels in cisplatin-sensitive KB-3-1 (KB) epidermoid cancer cells by the whole cell patch-clamp method. A cation channel in KB cells, activated by hypotonic stress, was identified as the Ca2+-activated, intermediate-conductance K+ (IK1) channel on the basis of its requirement for intracellular Ca2+, its blockage by the blockers clotrimazole and triarylmethane-34, and its suppression by a dominant-negative construct. Activity of this channel was not observed in KCP-4 cells, a cisplatin-resistant cell line derived from KB cells, and its molecular expression, observed by semiquantitative RT-PCR and immunostaining, appeared much reduced. Cell volume measurements confirmed a physiological role for the IK1 channel as a component of the volume-regulatory machinery in KB cells. A possible role of the IK1 channel in cisplatin-induced apoptosis was investigated. It was found that clotrimazole and triarylmethane-34 inhibited a cisplatin-induced decrease in cell viability and increase in caspase-3/7 activity, whereas 1-ethyl-2-benzimidazolinone, an activator of the channel, had the opposite effect. Thus IK1 channel activity appears to mediate, at least in part, the response of KB cells to cisplatin treatment.

MCF-7/VDR: A new vitamin D resistant cell line

2001 ◽  
Vol 82 (3) ◽  
pp. 422-436 ◽  
Author(s):  
Christina M�rk Hansen ◽  
Lili Rohde ◽  
Mogens W. Madsen ◽  
Dann Hansen ◽  
Kay W. Colston ◽  
...  
Keyword(s):  
Vitamin D ◽  
Cell Line ◽  
Resistant Cell ◽  
Resistant Cell Line ◽  
Mcf 7

scholarly journals Rps15a Imparts Chemoresistance by Regulating Cd44 Expression and Cell Stemness in Esophageal Squamous Cell Carcinoma

2021 ◽  
Author(s):  
Pengjun Zhou ◽  
Xiaoping Wang ◽  
Ziyao Li ◽  
Yifei Wang ◽  
Rong Zhang
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Drug Efficacy ◽  
Resistant Cell ◽  
Resistant Cell Line ◽  
Chemotherapeutic Drugs ◽  
Induced Apoptosis ◽  
Chemotherapy Efficacy

Abstract Chemotherapy is one of the effective ways to treat esophageal squamous cell carcinoma (ESCC), but the development of chemoresistance during chemotherapy lowers drug efficacy. Although previous studies have shown that the ribosomal protein S15A (RPS15A) involved in the progression and overall survival of malignancies, its function in chemoresistance is unknown. This study sought to elucidate the function of RPS15A in chemoresistance in ESCC. Our results show that knocking down or overexpressing RPS15A in ESCC cell lines can significantly change the sensitivity of chemotherapeutic drugs and affect cisplatin-induced apoptosis. Moreover, an increase in chemotherapeutic drug concentration leads to increased expression of RPS15A and CD44 proteins. When we utilized the ESCC cisplatin-resistant cell line to corroborate our findings, we found that the levels of RPS15A and CD44 proteins were substantially greater in daughter than parental cells. Subsequent experiments indicated that RPS15A modulated chemoresistance by controlling the expression of CD44 and the cell stemness in ESCC. Hence, our data suggest that RPS15A participates in the chemoresistance in ESCC by controlling the expression of CD44 and regulating cell stemness. Taken together, our study provides plausible mechanisms for RPS15A-mediated chemoresistance in ESCC cells and suggests that the inhibition of the RPS15A/CD44 pathway may be a potential target for improving chemotherapy efficacy.

MiR-765 Regulates Breast Cancer Cell Proliferation, Apoptosis, and Adriamycin Resistance Through Targeting Epithelial Membrane Protein 3

2020 ◽  
Vol 10 (8) ◽  
pp. 1193-1198
Author(s):  
Siyi Li ◽  
Hongjuan Peng ◽  
Jianwen Li
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Membrane Protein ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Resistant Cell ◽  
Resistant Cell Line ◽  
Cancer Cell Proliferation ◽  
Breast Cancer Cell Proliferation ◽  
Mcf 7

Epithelial membrane protein 3 (EMP3) regulates cell proliferation, differentiation, and apoptosis. Bioinformatics analysis revealed that miR-765 had complimentary sequence with the 3 -URT of EMP3 mRNA. miR-765 regulates EMP3 and influences breast cancer cell behaviors. However, it is unclear whether this regulation plays a role in affecting drug resistance. Our study assessed miR765's role in EMP3 expression and adriamycin (ADM) resistance of breast cancer. ADM resistant cell line MCF-7/ADM was established and assigned into miR-NC group, miR-765 mimic group, siRNA-NC group, and siRNA-EMP3 group followed by analysis of cell proliferation and apoptosis. miR-765 targets EMP3. The miR-765 level and apoptosis rate in MCF-7/ADM cells were significantly lower, while EMP3 level and cell proliferation were higher than MCF-7 cells. miR-765 mimic or siRNA-EMP3 significantly downregulated EMP3, weakened cell proliferation, increased apoptosis, and decreased ADM resistance. MiR-765 and EMP3 involves in ADM resistance of breast cancer cells. Up-regulation of miR-765 inhibits breast cancer cell proliferation and reduces ADM resistance via regulating EMP3.

scholarly journals Thrombospondin-1 Receptor CD47 Overexpression Contributes to P-Glycoprotein-Mediated Multidrug Resistance Against Doxorubicin in Thyroid Carcinoma FTC-133 Cells

2020 ◽  
Vol 10 ◽  
Author(s):  
Marie-Pierre Courageot ◽  
Laurent Duca ◽  
Laurent Martiny ◽  
Emmanuelle Devarenne-Charpentier ◽  
Hamid Morjani ◽  
...  
Keyword(s):  
Multidrug Resistance ◽  
Acquired Resistance ◽  
Resistant Cell ◽  
Resistant Cell Line ◽  
Rt Pcr ◽  
Jnk Pathway ◽  
P Glycoprotein ◽  
Thrombospondin 1 ◽  
Induced Apoptosis ◽  
Jnk Activation

It is now admitted that in addition to acquired resistance, the tumor microenvironment contributes to the development of chemo-resistance and malignant progression. In a previous study, we showed that Dox induced apoptosis in FTC-133 cells by trigging JNK pathway. This process was accompanied by a decrease of thrombospondin-1 (TSP-1) expression. Moreover, exogenous TSP-1 or its C-terminal-derived peptide interact with receptor CD47 and are able to protect FTC-133 cells against Dox-induced apoptosis. Here, we investigated the involvement of TSP-1/CD47 interaction in a context of acquired multidrug resistance in FTC-133 cells. To that end, we established a Dox-resistant cell line (FTC-133R cells) which developed a resistance against Dox-induced apoptosis. Cell viability was evaluated by Uptiblue assay, nuclear Dox was measured by microspectrofluorimetry, caspase activity was measured by fluorescence of cleaved caspase-3 substrate, gene expression was evaluated by RT-PCR and protein expression was examined by western-blot. Our results showed that FTC-133R overexpressed the P-gp and were 15-fold resistant to Dox. JNK phosphorylation and Dox-induced apoptosis were reduced in FTC-133R cells. Expression of CD47 was increased in FTC-133R cells but TSP-1 expression presented similar levels in two cell lines. VPL restored Dox nuclear uptake and FTC-133R cell sensitivity to apoptosis and induced a decrease in CD47 mRNA expression. Moreover, knockdown of CD47 in FTC-133R cells induced an increase in JNK activation and sensitized FTC-133R cells to Dox. Our data suggest that CD47 is able to contribute to the protection of FTC-133R cells against Dox-induced apoptosis and/or to potentiate the acquired Dox resistance.

scholarly journals Lack of ceramide generation and altered sphingolipid composition are associated with drug resistance in human ovarian carcinoma cells

2006 ◽  
Vol 395 (2) ◽  
pp. 311-318 ◽  
Author(s):  
Alessandro Prinetti ◽  
Danilo Millimaggi ◽  
Sandra D'Ascenzo ◽  
Matilda Clarkson ◽  
Arianna Bettiga ◽  
...  
Keyword(s):  
Ovarian Carcinoma ◽  
Cell Line ◽  
Resistant Cell ◽  
Resistant Cell Line ◽  
Acid Sphingomyelinase ◽  
Ovarian Carcinoma Cell Line ◽  
Ganglioside Content ◽  
Human Ovarian Carcinoma ◽  
Induced Apoptosis ◽  
I Cells

PTX (Paclitaxel®) is an antimitotic agent used in the treatment of a number of major solid tumours, particularly in breast and ovarian cancer. This study was undertaken to gain insight into the molecular alterations producing PTX resistance in ovarian cancer. PTX treatment is able to induce apoptosis in the human ovarian carcinoma cell line, CABA I. PTX-induced apoptosis in CABA I cells was accompanied by an increase in the cellular Cer (ceramide) levels and a decrease in the sphingomyelin levels, due to the activation of sphingomyelinases. The inhibition of acid sphingomyelinase decreased PTX-induced apoptosis. Under the same experimental conditions, PTX had no effect on Cer and sphingomyelin levels in the stable PTX-resistant ovarian carcinoma cell line, CABA-PTX. The acquisition of the PTX-resistant phenotype is accompanied by unique alterations in the complex sphingolipid pattern found on lipid extraction. In the drug-resistant cell line, the levels of sphingomyelin and neutral glycosphingolipids were unchanged compared with the drug-sensitive cell line. The ganglioside pattern in CABA I cells is more complex compared with that of CABA-PTX cells. Specifically, we found that the total ganglioside content in CABA-PTX cells was approximately half of that in CABA I cells, and GM3 ganglioside content was remarkably higher in the drug-resistant cell line. Taken together our findings indicate that: i) Cer generated by acid sphingomyelinase is involved in PTX-induced apoptosis in ovarian carcinoma cells, and PTX-resistant cells are characterized by their lack of increased Cer upon drug treatment, ii) PTX resistance might be correlated with an alteration in metabolic Cer patterns specifically affecting cellular ganglioside composition.

scholarly journals MicroRNA-222 promotes drug resistance to doxorubicin in breast cancer via regulation of miR-222/bim pathway

2019 ◽  
Vol 39 (7) ◽  
Author(s):  
Hong Dai ◽  
Ling-yun Xu ◽  
Qi Qian ◽  
Qiu-wei Zhu ◽  
Wei-xian Chen
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Malignant Tumors ◽  
Clinical Problem ◽  
Resistant Cell ◽  
Resistant Cell Line ◽  
Caspase Pathway ◽  
Resistance To Doxorubicin ◽  
Mcf 7

Abstract Resistance to doxorubicin (DOX) is the most common clinical problem in breast cancer therapy, and the underlying molecular mechanism remains to be investigated. MicroRNAs (miRNAs) exhibit important regulatory functions in various malignant tumors including breast cancer. The aim of the present study was to find the relationship between miR-222 and DOX resistance. We found that miR-222 was highly expressed in patients’ serum and DOX-resistant cell line MCF-7-R and that miR-222 could promote proliferation and migration of breast cancer cells. Our results also showed that inhibition of miR-222 in MCF-7-R significantly increased Bcl-2 interacting mediator (Bim) expression both in mRNA and protein levels by using quantitative real-time PCR (qRT-PCR) and Western blot. MTT and flow cytometry suggested that lower expressed miR-222 enhanced apoptosis and decreased IC50 of MCF-7-R cells. Conversely, in MCF-7 cells transfected with miR-222 mimics, up-regulation of miR-222 was associated with decreased Bim level accompanied by less apoptosis and higher IC50. Moreover, miR-222 inhibitors reversed DOX resistance via miR-222-Bim-caspase pathway. Collectively, these data first elucidated that miR-222 could function as an oncogene and was able to reduce the sensitivity of breast cancer cells to DOX through miR-222-Bim-caspase pathway, which provided a potential target to increase DOX sensitivity in clinical breast cancer treatment.

TIMP-1 protects MCF-7 breast cancer cells from paclitaxel-induced apoptosis by decreasing the stability of cyclin B1

2009 ◽  
Vol 63 (5) ◽  
pp. 324
Author(s):  
Ting Wang ◽  
Jing-Huan Lv ◽  
Xiong-Fei Zhang ◽  
Chao-Jun Li ◽  
Xiao Han ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Cyclin B1 ◽  
The Stability ◽  
Induced Apoptosis ◽  
Mcf 7
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