Apoptotic Effects of Resveratrol via mTOR and COX-2 Signal Pathways in MCF-7 Breast Cancer Cells

Lee, Sol Hwa; Lee, Hye yeon; Park, Song‐Yi; Park, Ock Jin; Kim, Young Min

doi:10.5352/jls.2011.21.9.1288

Cited by 2 publications

(3 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Also, this combination selectively inhibited COX-2 but not COX-1 (Lev-Ari, Strier et al, 2005;Lev-Ari, Zinger et al, 2005). S. H. Lee et al (2012) showed that curcumin inhibits COX-2 and its downstream genes including vasodilator-stimulated phosphoprotein, leading to apoptosis induction in MCF-7 cells. The authors showed that COX-2 suppression by curcumin was mediated through AMP-activated protein kinase (AMPK).…”

Section: Inhibition Of Cox-2mentioning

confidence: 99%

Mechanisms of apoptosis modulation by curcumin: Implications for cancer therapy

Mortezaee

Salehi

Mirtavoos-Mahyari

et al. 2019

Journal Cellular Physiology

271

154

View full text Add to dashboard Cite

Cancer incidences are growing and cause millions of deaths worldwide. Cancer therapy is one of the most important challenges in medicine. Improving therapeutic outcomes from cancer therapy is necessary for increasing patients’ survival and quality of life. Adjuvant therapy using various types of antibodies or immunomodulatory agents has suggested modulating tumor response. Resistance to apoptosis is the main reason for radioresistance and chemoresistance of most of the cancers, and also one of the pivotal targets for improving cancer therapy is the modulation of apoptosis signaling pathways. Apoptosis can be induced by intrinsic or extrinsic pathways via stimulation of several targets, such as membrane receptors of tumor necrosis factor‐α and transforming growth factor‐β, and also mitochondria. Curcumin is a naturally derived agent that induces apoptosis in a variety of different tumor cell lines. Curcumin also activates redox reactions within cells inducing reactive oxygen species (ROS) production that leads to the upregulation of apoptosis receptors on the tumor cell membrane. Curcumin can also upregulate the expression and activity of p53 that inhibits tumor cell proliferation and increases apoptosis. Furthermore, curcumin has a potent inhibitory effect on the activity of NF‐κB and COX‐2, which are involved in the overexpression of antiapoptosis genes such as Bcl‐2. It can also attenuate the regulation of antiapoptosis PI3K signaling and increase the expression of MAPKs to induce endogenous production of ROS. In this paper, we aimed to review the molecular mechanisms of curcumin‐induced apoptosis in cancer cells. This action of curcumin could be applicable for use as an adjuvant in combination with other modalities of cancer therapy including radiotherapy and chemotherapy.

show abstract

Section: Inhibition Of Cox-2mentioning

confidence: 99%

Mechanisms of apoptosis modulation by curcumin: Implications for cancer therapy

Mortezaee

Salehi

Mirtavoos-Mahyari

et al. 2019

Journal Cellular Physiology

271

154

View full text Add to dashboard Cite

show abstract

“…Regulation of mTORC1 by phosphorylation of TSC2 induces cell survival and growth [5]. Also, inhibition of the Akt/mTOR signaling pathway induces decrease in COX-2 expression [14,40]. Furthermore, the inactive form of GSK-3β cannot degrade βcatenin, and its presence leads to β-catenin translocation to the nucleus.…”

Section: Cme Treatment Regulates Expression Of Apoptosis-related Prot...mentioning

confidence: 99%

“…COX-2 expression is controlled by both the Akt/ mTOR and GSK-3β/β-catenin signaling pathways [10][11][12][13]. COX-2 inhibition leads to apoptosis through regulation of Bcell lymphoma 2 (Bcl-2) and pro-apoptotic proteins such as Bax and Bak, and induces G1 cell cycle arrest through decreasing cyclin D1 activity [10,[14][15][16].…”

Section: Introductionmentioning

confidence: 99%

Extracts from Cnidium monnieri (L.) Cusson Induces Apoptosis and G1 Cell Cycle Arrest through Reducing COX-2 Expression by Regulating the Akt/GSK-3β Signaling Pathways

Lim,

Youk,

Kim

2023

KSBB

View full text Add to dashboard Cite

Cnidium monnieri (L.) Cusson is an annual plant distributed in China and Korea. The fruit of C. monnieri is used as a medicinal herb and is effective for the treatment of carbuncle and pain in the female genitalia. In this study, we investigated the effects on apoptosis and cell cycle arrest by ethanol extracts from C. monnieri (CME) in HT-29 colon cancer cells. The results of MTT and LDH assays demonstrated the antiproliferative and cytotoxic effects of CME. Also, the number of apoptotic bodies and the apoptotic rate were increased by CME. Moreover, cell cycle arrest occurred in the G1 phase by CME. Akt down-regulates various proteins, such as TSC2 and GSK-3β. Transcription of the cyclooxygenase-2 (COX-2) gene is regulated by the GSK-3β/β-catenin signaling pathway. Overexpression of COX-2 induces production of the anti-apoptotic protein, Bcl-2. To confirm the regulatory effect on signaling proteins of CME, we used Western blot analysis in vivo and in vitro. The results showed that, the expression levels of p-Akt, p-TSC2, p-mTOR, p-GSK-3β, β-catenin, COX-2, Bcl-2 family members, and caspase-3 were regulated by CME. Treatment with specific inhibitors showed that CMEinduced apoptosis occurred through regulation of COX-2 expression via both the Akt/GSK-3β/mTOR and Akt/GSK-3β/β-catenin signaling pathways.

show abstract

Apoptotic Effects of Resveratrol via mTOR and COX-2 Signal Pathways in MCF-7 Breast Cancer Cells

Cited by 2 publications

References 20 publications

Mechanisms of apoptosis modulation by curcumin: Implications for cancer therapy

Mechanisms of apoptosis modulation by curcumin: Implications for cancer therapy

Extracts from Cnidium monnieri (L.) Cusson Induces Apoptosis and G1 Cell Cycle Arrest through Reducing COX-2 Expression by Regulating the Akt/GSK-3β Signaling Pathways

Contact Info

Product

Resources

About