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cancer
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505522 occurrences (No.25 in the rank) during 5 years in the PubMed. [cache]
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[frequency of next (right) word to cancer]
505522 occurrences (No.25 in the rank) during 5 years in the PubMed. [cache]
| 177) We focused on Δ2-troglitazone (Δ2-TGZ), a PPARγ inactive TZD that affects breast cancer cell viability. |
| PMID:24293218 DOI:10.1002/mc.22109 |
| 2015 Molecular carcinogenesis |
| * PPARγ-inactive Δ2-troglitazone independently triggers ER stress and apoptosis in breast cancer cells. |
| - Our aim was to better understand peroxisome proliferator-activated receptor gamma (PPARγ)-independent pathways involved in anti-cancer effects of thiazolidinediones (TZDs). We focused on Δ2-troglitazone (Δ2-TGZ), a PPARγ inactive TZD that affects breast cancer cell viability. Appearance of TUNEL positive cells, changes in mitochondrial membrane potential, cleavage of poly(ADP-ribose) polymerase (PARP)-1 and caspase-7 revealed that apoptosis occurred in both hormone-dependent MCF7 and hormone-independent MDA-MB-231 breast cancer cells after 24 and 48 h of treatment. A microarray study identified endoplasmic reticulum (ER) stress as an essential cellular function since many genes involved in ER stress were upregulated in MCF7 cells following Δ2-TGZ treatment. Δ2-TGZ-induced ER stress was further confirmed in MCF7 cells by phosphorylation of pancreatic endoplasmic reticulum kinase-like endoplasmic reticulum kinase (PERK) and its target eIF2α after 1.5 h, rapid increase in activating transcription factor (ATF) 3 mRNA levels, splicing of X-box binding protein 1 (XBP1) after 3 h, accumulation of binding immunogloblulin protein (BiP) and CCAAT-enhancer-binding protein homologous protein (CHOP) after 6 h. Immunofluorescence microscopy indicated that CHOP was relocalized to the nucleus of treated cells. Similarly, in MDA-MB-231 cells, overexpression of ATF3, splicing of XBP1, and accumulation of BiP and CHOP were observed following Δ2-TGZ treatment. In MCF7 cells, knock-down of CHOP or the inhibition of c-Jun N-terminal kinase (JNK) did not impair cleavage of PARP-1 and caspase-7. Altogether, our results show that ER stress is an early response of major types of breast cancer cells to Δ2-TGZ, prior to, but not causative of apoptosis. |
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| (1)65 *null* | (14)6  therapy |
(27)3 of |
(40)2 epigenetics |
| (2)48 cells |
(15)6 tissues |
(28)3 patients, |
(41)2 growth |
| (3)33 and |
(16)5 cells, |
(29)3 research |
(42)2 initiation |
| (4)32 cell |
(17)5 progression |
(30)3 was |
(43)2 prevention |
| (5)23 patients |
(18)5 registries |
(31)2 (GC) |
(44)2 registry |
| (6)15 in |
(19)4 at |
(32)2 biology |
(45)2 study |
| (7)14 is |
(20)4 deaths |
(33)2 but |
(46)2 susceptibility |
| (8)12 risk |
(21)4 has |
(34)2 can |
(47)2 than |
| (9)12 screening |
(22)4 mortality |
(35)2 care |
(48)2 treated |
| (10)12 stem |
(23)3 (CRC) |
(36)2 development |
(49)2 treatment |
| (11)9 survivors |
(24)3 as |
(37)2 diagnostic |
(50)2 using |
| (12)7 with |
(25)3 cases |
(38)2 drug |
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| (13)6 are |
(26)3 metabolism |
(39)2 drugs |
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--- WordNet output for cancer ---