N-acetyl cysteine mitigates curcumin-mediated telomerase inhibition through rescuing of Sp1 reduction in A549 cells

Hsin, I.; Sheu, Gwo‐Tarng; Chen, Hung-Hsuan; Chiu, Ling‐Yen; Wang, Horng-Dar; Chan, Hsiu‐Wen; Hsu, Chung-Ping

doi:10.1016/j.mrfmmm.2010.03.011

Cited by 43 publications

(36 citation statements)

References 40 publications

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“…ROS have been shown previously to induce proteasome-mediated reduction of Sp1 levels through reduction of Sp1 O-glycosylation (Kim et al, 2012), whereas N-acetyl cysteine (NAC) has been shown to mitigate this effect (Hsin et al, 2010). Thus, we next measured ROS levels in CerS2 null astrocytes, which were elevated ∼fourfold (Fig.…”

Section: Cme Is Attenuated By the Oxidative State Of The Cellsmentioning

confidence: 96%

Oxidative stress elicited by modifying the ceramide acyl chain length reduces the rate of clathrin-mediated endocytosis

Volpert

Ben‐Dor

Tarcic

et al. 2017

Journal of Cell Science

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Sphingolipids modulate clathrin-mediated endocytosis (CME) by altering the biophysical properties of membranes. We now examine CME in astrocytes cultured from ceramide synthase 2 (CerS2) null mice, which have an altered sphingolipid acyl chain composition. The rate of endocytosis of low-density lipoprotein and transferrin, which are internalized via CME, was reduced in CerS2 null astrocytes, although the rate of caveolin-mediated endocytosis was unaltered. Levels of clathrin heavy chain were increased, which was due to decreased levels of Hsc70 (also known as HSPA8), a protein involved in clathrin uncoating. Hsc70 levels were decreased because of lower levels of binding of Sp1 to position −68 in the Hsc70 promoter. Levels of Sp1 were downregulated due to oxidative stress, which was elevated fourfold in CerS2 null astrocytes. Furthermore, induction of oxidative stress in wild-type astrocytes decreased the rate of CME, whereas amelioration of oxidative stress in CerS2 null astrocytes reversed the decrease. Our data are consistent with the notion that sphingolipids not only change membrane biophysical properties but also that changes in their composition can result in downstream effects that indirectly impinge upon a number of cellular pathways, such as CME.

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Section: Cme Is Attenuated By the Oxidative State Of The Cellsmentioning

confidence: 96%

Oxidative stress elicited by modifying the ceramide acyl chain length reduces the rate of clathrin-mediated endocytosis

Volpert

Ben‐Dor

Tarcic

et al. 2017

Journal of Cell Science

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“…The detailed steps of lentivirus production and infection have been described previously. 63 Individual clones were identified by their unique TRC number: shLuc TRCN0000072246 for vector control targeted to luciferase, shLC3 (91) (LC3.91) TRCN0000243391 (corresponding sequence: AGC GAG TTG GTC AAG ATC ATC) targeted to LC3 (I and II), shBECN1 (49) TRCN0000033549 (corresponding sequence: CCC GTG GAA TGG AAT GAG ATT) targeted to BECN1, shATG5 (74) TRCN0000151474 (corresponding sequence: CCT TTC ATT CAG AAG CTG TTT) targeted to ATG5.…”

Section: Vsv-g Pseudotyped Lentivirus-shrna Production and Infectionmentioning

confidence: 99%

Suberoylanilide hydroxamic acid (SAHA) causes tumor growth slowdown and triggers autophagy in glioblastoma stem cells

et al. 2013

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“…Curcumin has been shown to inhibit activities of the proteasome in certain cancer cells [26] ; however, Fossey et al found that no evidence for this activity after treating the OSA cell lines with curcumin at the doses and time points examined [27] . Moreover, previous studies reported that the decreased expression of Sp1 in A549 cells and cyclin E in MCF-7 cells by curcumin were reversed by proteasome inhibitors, suggesting the role of ubiquitin-dependent proteasomal pathway [28][29] . In the present study, we explored the mechanism by which curcumin reduces AP-2γ protein levels in NTera-2 cells.…”

Section: Discussionmentioning

confidence: 89%

Curcumin inhibits AP-2γ-induced apoptosis in the human malignant testicular germ cells in vitro

Zhou

Zhao

et al. 2013

Acta Pharmacol Sin

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Aim: To investigate the effects of curcumin on proliferation and apoptosis in testicular cancer cells in vitro and to investigate its molecular mechanisms of action. Methods: NTera-2 human malignant testicular germ cell line and F9 mouse teratocarcinoma stem cell line were used. The anti-proliferative effect was examined using MTT and colony formation assays. Hoechst 33258 staining, TUNEL and Annexin V-FITC/PI staining assays were used to analyze cell apoptosis. Protein expression was examined with Western blot analysis and immunocytochemical staining. Results: Curcumin (5, 10 and 15 μmol/L) inhibited the viability of NTera-2 cells in dose-and time-dependent manners. Curcumin significantly inhibited the colony formation in both NTera-2 and F9 cells. Curcumin dose-dependently induced apoptosis of NTera-2 cells by reducing FasL expression and Bcl-2-to-Bax ratio, and activating caspase-9, -8 and -3. Furthermore, curcumin dose-dependently reduced the expression of AP transcription factor AP-2γ in NTera-2 cells, whereas the pretreatment with the proteasome inhibitor MG132 blocked both the curcumin-induced reduction of AP-2γ and antiproliferative effect. Curcumin inhibited ErbB2 expression, and decreased the phosphorylation of Akt and ERK in NTera-2 cells. Conclusion: Curcumin induces apoptosis and inhibits proliferation in NTera-2 cells via the inhibition of AP-2γ-mediated downstream cell survival signaling pathways.

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N-acetyl cysteine mitigates curcumin-mediated telomerase inhibition through rescuing of Sp1 reduction in A549 cells

Cited by 43 publications

References 40 publications

Oxidative stress elicited by modifying the ceramide acyl chain length reduces the rate of clathrin-mediated endocytosis

Oxidative stress elicited by modifying the ceramide acyl chain length reduces the rate of clathrin-mediated endocytosis

Suberoylanilide hydroxamic acid (SAHA) causes tumor growth slowdown and triggers autophagy in glioblastoma stem cells

Curcumin inhibits AP-2γ-induced apoptosis in the human malignant testicular germ cells in vitro

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