Cyclooxygenase-2 Inducing Mcl-1-dependent Survival Mechanism in Human Lung Adenocarcinoma CL1.0 Cells

Lin, Jaw–Town; Lee, Rung-Chi; Yang, Pan‐Chyr; Ho, Feng-Ming; Kuo, Min-Liang

doi:10.1074/jbc.m107829200

Cited by 174 publications

(126 citation statements)

References 26 publications

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“…32,33 Furthermore, several studies have established a direct role for Cox-2 in rendering cells resistant to apoptosis by upregulating the expression of Mcl-1 through activation of the PI 3-kinase/Akt-dependent pathway. 18,21 In the present study, cytoplasmic immunoreactivity for Cox-2 was observed in retinal ganglion cells, in the retinal pigment epithelial cells, and in the pigmented and nonpigmented layers of the ciliary body epithelium in diabetic and nondiabetic retinas, confirming previous reports. 31,[34][35][36] The expression of the antiapoptotic molecules Akt, Cox-2, and Mcl-1 in retinal ganglion cells may reflect the fact that neurons tend to be maintained for the entire life span of an individual.…”

Section: Discussionsupporting

confidence: 92%

“…[11][12][13][14][15][16] Several studies showed that Cox-2 functions as a survival factor by protecting cells from apoptosis. [17][18][19][20][21] Overexpression of Mcl-1, a member of the Bcl-2 family, 22 delays apoptosis by a broad array of agents. 18,21,[23][24][25][26] Bad is a proapoptotic member of the Bcl-2 gene family that promotes apoptosis by binding to and inhibiting functions of antiapoptotic proteins Bcl-2 and Bcl-xL.…”

mentioning

confidence: 99%

“…[17][18][19][20][21] Overexpression of Mcl-1, a member of the Bcl-2 family, 22 delays apoptosis by a broad array of agents. 18,21,[23][24][25][26] Bad is a proapoptotic member of the Bcl-2 gene family that promotes apoptosis by binding to and inhibiting functions of antiapoptotic proteins Bcl-2 and Bcl-xL. 10,27 Mitochondria play a key role in the control of apoptotic cell death.…”

mentioning

confidence: 99%

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Expression of antiapoptotic and proapoptotic molecules in diabetic retinas

El‐Asrar

Dralands

Missotten

et al. 2006

Eye

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Section: Discussionsupporting

confidence: 92%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Expression of antiapoptotic and proapoptotic molecules in diabetic retinas

El‐Asrar

Dralands

Missotten

et al. 2006

Eye

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“…Overexpression of COX-2 is often observed in many types of cancer cells and results in an increase of cell survival (Lin et al, 2001) and metastasis (Tsujii et al, 1997) and a reduction of apoptosis (Nzeako et al, 2002). COX inhibition by NSAIDs at the protein level is likely to be closely related to their anti-tumorigenic effects.…”

Section: Discussionmentioning

confidence: 99%

Molecular characterisation of canine nonsteroidal anti-inflammatory drug-activated gene (NAG-1)

Yamaguchi

Whitlock

Liggett

et al. 2008

The Veterinary Journal

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Nonsteroidal anti-inflammatory drug (NSAID)-activated gene (NAG-1), a divergent member of the transforming growth factor β superfamily, was previously identified as a gene induced by several anti-tumorigenic compounds, including NSAIDs and peroxisome proliferator-activated receptor γ (PPARγ) ligands in humans. In this study, canine NAG-1 was characterised from a canine genomic database. Gene induction by some NSAIDs and PPARγ ligands was demonstrated in canine osteosarcoma cell lines. Phylogenetic analysis indicates that canine NAG-1 is more homologous with the corresponding mouse and rat genes than with human NAG-1. Expression of canine NAG-1 was increased by treatment with piroxicam and SC-560 (NSAIDs) and the PPARγ ligand rosiglitazone. This study demonstrates that canine NAG-1 is up-regulated by some anti-tumorigenic compounds in osteosarcoma cell lines and may provide an important target of chemotherapy in canine cancer.

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“…In SCLC cell lines, Bcl-2 family members have been described as important factors in chemotherapeutic drug resistance and therefore downregulation of Bcl-2 family members with an NSAID can be an interesting modality to circumvent drug resistance (Sartorius and Krammer, 2002). Human lung adenocarcinoma cells, exposed to NSAIDs showed an effective reduction of the antiapoptosis Bcl-2 family member Mcl-1 (Lin et al, 2001).…”

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confidence: 99%

Indomethacin-induced activation of the death receptor-mediated apoptosis pathway circumvents acquired doxorubicin resistance in SCLC cells

et al. 2005

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Small-cell lung cancers (SCLCs) initially respond to chemotherapy but are often resistant at recurrence. A potentially new method to overcome resistance is to combine classical chemotherapeutic drugs with apoptosis induction via tumour necrosis factor (TNF) death receptor family members such as Fas. The doxorubicin-resistant human SCLC cell line GLC 4 -Adr and its parental doxorubicinsensitive line GLC 4 were used to analyse the potential of the Fas-mediated apoptotic pathway and the mitochondrial apoptotic pathway to modulate doxorubicin resistance in SCLC. Western blotting showed that all proteins necessary for death-inducing signalling complex formation and several inhibitors of apoptosis were expressed in both lines. The proapototic proteins Bid and caspase-8, however, were higher expressed in GLC 4 -Adr. In addition, GLC 4 -Adr expressed more Fas (3.1x) at the cell membrane. Both lines were resistant to anti-Fas antibody, but plus the protein synthesis inhibitor cycloheximide anti-Fas antibody induced 40% apoptosis in GLC 4 -Adr. Indomethacin, which targets the mitochondrial apoptotic pathway, induced apoptosis in GLC 4 -Adr but not in GLC 4 cells. Surprisingly, in GLC 4 -Adr indomethacin induced caspase-8 and caspase-9 activation as well as Bid cleavage, while both caspase-8 and caspase-9 specific inhibitors blocked indomethacin-induced apoptosis. In GLC 4 -Adr, doxorubicin plus indomethacin resulted in elevated caspase activity and a 2.7-fold enhanced sensitivity to doxorubicin. In contrast, no effect of indomethacin on doxorubicin sensitivity was observed in GLC 4 . Our findings show that indomethacin increases the cytotoxic activity of doxorubicin in a doxorubicin-resistant SCLC cell line partly via the death receptor apoptosis pathway, independent of Fas.

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Cyclooxygenase-2 Inducing Mcl-1-dependent Survival Mechanism in Human Lung Adenocarcinoma CL1.0 Cells

Cited by 174 publications

References 26 publications

Expression of antiapoptotic and proapoptotic molecules in diabetic retinas

Expression of antiapoptotic and proapoptotic molecules in diabetic retinas

Molecular characterisation of canine nonsteroidal anti-inflammatory drug-activated gene (NAG-1)

Indomethacin-induced activation of the death receptor-mediated apoptosis pathway circumvents acquired doxorubicin resistance in SCLC cells

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