Preventing chemoresistance of human breast cancer cell line, MCF-7 with celecoxib

Chen, Chen; Shen, Hui; Yang, Jing; Chen, Qiao Yun; Xu, Wen

doi:10.1007/s00432-010-0854-3

Cited by 29 publications

(20 citation statements)

References 28 publications

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“…Relevant studies have demonstrated that COX-2 inhibitors increase the sensitivity of cancer cells to chemotherapeutics by regulating the activity of P-gp [12], [13]. It has been found that celecoxib, a selective COX-2 inhibitor, may downregulate P-gp expression in cancer cells by suppressing the expression of transcription factors such as NF-κB [14], [15]. Several studies indicated that the MDR-1 gene may contain DNA binding sites for transcription factor NF-κB [16], [17].…”

Section: Introductionmentioning

confidence: 99%

Sinomenine Sensitizes Multidrug-Resistant Colon Cancer Cells (Caco-2) to Doxorubicin by Downregulation of MDR-1 Expression

et al. 2014

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Chemoresistance in multidrug-resistant (MDR) cells over expressing P-glycoprotein (P-gp) encoded by the MDR1 gene, is a major obstacle to successful chemotherapy for colorectal cancer. Previous studies have indicated that sinomenine can enhance the absorption of various P-gp substrates. In the present study, we investigated the effect of sinomenine on the chemoresistance in colon cancer cells and explored the underlying mechanism. We developed multidrug-resistant Caco-2 (MDR-Caco-2) cells by exposure of Caco-2 cells to increasing concentrations of doxorubicin. We identified overexpression of COX-2 and MDR-1 genes as well as activation of the NF-κB signal pathway in MDR-Caco-2 cells. Importantly, we found that sinomenine enhances the sensitivity of MDR-Caco-2 cells towards doxorubicin by downregulating MDR-1 and COX-2 expression through inhibition of the NF-κB signaling pathway. These findings provide a new potential strategy for the reversal of P-gp-mediated anticancer drug resistance.

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Section: Introductionmentioning

confidence: 99%

Sinomenine Sensitizes Multidrug-Resistant Colon Cancer Cells (Caco-2) to Doxorubicin by Downregulation of MDR-1 Expression

et al. 2014

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“…In the MCF7 breast cancer cell line, the interaction of celecoxib with these four chemotherapeutics was antagonistic, indicating that celecoxib is of little value when used in combination with antitumour drugs in the treatment of breast cancer. By contrast, other data indicate that celecoxib enhances the cytotoxicity of anticancer drugs in breast cancer cells (99,108). The interaction of celecoxib with etoposide, cisplatin and 5-FU was shown to be dependent on the cancer cell line employed, the drug type used and the incubation schedule.…”

Section: Combination Of Nsaids With Chemotherapeutic Drugs In Vitromentioning

confidence: 80%

Potency of non-steroidal anti-inflammatory drugs in chemotherapy

Hiľovská

Jendželovský

Fedoročko

2014

Molecular and Clinical Oncology

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“…Cyclooxygenase-2 (COX-2) and sphingosine kinase 2 (SphK2). It is thought that COX-2 inhibitors prevent the development of resistance to different cytostatics and that COX-2 overexpression induces increased multidrug resistance protein 1 (MRP1) expression in different cancer cells [99][100][101][102] . Schnitzer et al showed that COX-2 is upregulated under hypoxia in a HIF-1-independent fashion and sphingosine-1-phosphate (S1P) is responsible for COX-2 induction under hypoxia in A549 lung cancer cells 103 .…”

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confidence: 99%

Hypoxia-induced chemoresistance in cancer cells: The role of not only HIF-1

Doktorova

Hraběta

Khalil

et al. 2015

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

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Background. The aim of this review is to provide the information about molecular basis of hypoxia-induced chemoresistance, focusing on the possibility of diagnostic and therapeutic use. Results. Hypoxia is a common feature of tumors and represents an independent prognostic factor in many cancers. It is the result of imbalances in the intake and consumption of oxygen caused by abnormal vessels in the tumor and the rapid proliferation of cancer cells. Hypoxia-induced resistance to cisplatin, doxorubicin, etoposide, melphalan, 5-flouoruracil, gemcitabine, and docetaxel has been reported in a number of experiments. Adaptation of tumor cells to hypoxia has important biological effects. The most studied factor responsible for these effects is hypoxia-inducible factor-1 (HIF-1) that significantly contributes to the aggressiveness and chemoresistance of different tumors. The HIF-1 complex, induced by hypoxia, binds to target genes, thereby increasing the expression of many genes. In addition, the expression of hundreds of genes can be also decreased in response to hypoxia in HIF-1 dependent manner, but without the detection of HIF-1 in these genes' promoters. HIF-1 independent mechanisms for drug resistance in hypoxia have been described, however, they are still rarely reported. The first clinical studies focusing on diagnosis of hypoxia and on inhibition of hypoxia-induced changes in cancer cells are starting to yield results. Conclusions. The adaptation to hypoxia requires many genetic and biochemical responses that regulate one another. Hypoxia-induced resistance is a very complex field and we still know very little about it. Different approaches to circumvent hypoxia in tumors are under development.

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Preventing chemoresistance of human breast cancer cell line, MCF-7 with celecoxib

Cited by 29 publications

References 28 publications

Sinomenine Sensitizes Multidrug-Resistant Colon Cancer Cells (Caco-2) to Doxorubicin by Downregulation of MDR-1 Expression

Sinomenine Sensitizes Multidrug-Resistant Colon Cancer Cells (Caco-2) to Doxorubicin by Downregulation of MDR-1 Expression

Potency of non-steroidal anti-inflammatory drugs in chemotherapy

Hypoxia-induced chemoresistance in cancer cells: The role of not only HIF-1

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