Effect of β-Phenylethyl Isothiocyanate from Cruciferous Vegetables on Growth Inhibition and Apoptosis of Cervical Cancer Cells through the Induction of Death Receptors 4 and 5

Huong, Le Diem; Shim, Jae-Hyun; Choi, Kyoung-Ho; Shin, Ji‐Ae; Choi, Eui Yul; Kim, Hyungseop; Lee, Sook-Jeong; Kim, Sun-Ju; Cho, Nam-Pyo; Cho, Sung‐Dae

doi:10.1021/jf2006358

Cited by 42 publications

(46 citation statements)

References 43 publications

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“…Phenethyl isothiocyanate (PEITC) is an important compound obtained from cruciferous vegetables that is effective in numerous types of cancer, including prostate, breast, ovarian, oral and lung cancer (3)(4)(5)(6)(7). Several mechanisms, including the inhibition of cytochrome p450 enzymes, the induction of phase II detoxification enzymes (8) and the activation of death receptors 4 and 5 (9), are involved in the anti-tumor effects of PEITC. PEITC has also been shown to decrease the expression and function of the estrogen receptor (10).…”

Section: Introductionmentioning

confidence: 99%

Phenethyl isothiocyanate inhibits growth of human chronic myeloid leukemia K562 cells via reactive oxygen species generation and caspases

Wang¹,

Wei²,

Wang³

et al. 2014

Molecular Medicine Reports

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Abstract. Phenethyl isothiocyanate (PEITC), a potential cancer chemopreventive constituent of cruciferous vegetables, including watercress, has been reported to inhibit cancer cell growth by arresting the cell cycle and inducing apoptosis in various human cancer cell models. However, the role of PEITC in the inhibition of human chronic myeloid leukemia (CML) K562 cell growth and its underlying mechanisms have yet to be elucidated. In the present study, PEITC was found to induce cell death through the induction of reactive oxygen species (ROS) stress and oxidative damage. Heme oxygenase-1 (HO-1), which participates in the development of numerous tumors and the sensitivity of these tumors to chemotherapeutic drugs, plays a protective role by modulating oxidative injury. Therefore, the present study assessed the inhibitory effect of PEITC on K562 cells and whether HO-1 facilitated cell apoptosis and ROS generation. PEITC was found to suppress cell growth and cause apoptosis by promoting Fas and Fas ligand expression, increasing ROS generation and by the successive release of cytochrome c as well as the activation of caspase-9 and caspase-3. PEITC was also combined with the HO-1 inhibitor zinc protoporphyrin IX and the inducer hemin to assess whether HO-1 determines cell survival and ROS generation. The results of the present study suggest that PEITC may be a potential anti-tumor compound for CML therapy, and that HO-1 has a critical function in PEITC-induced apoptosis and ROS generation.

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Section: Introductionmentioning

confidence: 99%

Phenethyl isothiocyanate inhibits growth of human chronic myeloid leukemia K562 cells via reactive oxygen species generation and caspases

Wang¹,

Wei²,

Wang³

et al. 2014

Molecular Medicine Reports

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“…PEITC treated cervical cancer cells displayed a marked decrease in phosphorylated levels of (ERK)1/2. Moreover DR4 and DR5 were remarkably enhanced after treatment of cervical cancer cells with PEITC (Huong et al, 2011).…”

Section: Phenethyl Isothiocyanatementioning

confidence: 93%

Dealing Naturally with Stumbling Blocks on Highways and Byways of TRAIL Induced Signaling

Rana¹,

Attar²,

Qureshi³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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In-depth analysis of how TRAIL signals through death receptors to induce apoptosis in cancer cells using high throughput technologies has added new layers of knowledge. However, the wealth of information has also highlighted the fact that TRAIL induced apoptosis may be impaired as evidenced by experimental findings obtained from TRAIL resistant cancer cell lines. Overwhelmingly, increasing understanding of TRAIL mediated apoptosis has helped in identifying synthetic and natural compounds which can restore TRAIL induced apoptosis via functionalization of either extrinsic or intrinsic pathways. Increasingly it is being realized that biologically active phytochemicals modulate TRAIL induced apoptosis, as evidenced by cell-based studies. In this review we have attempted to provide an overview of how different phytonutrients have shown efficacy in restoring apoptosis in TRAIL resistant cancer cells. We partition this review into how the TRAIL mediated signaling landscape has broadened over the years and how TRAIL induced signaling machinery crosstalks with autophagic protein networks. Subsequently, we provide a generalized view of considerable biological activity of coumarins against a wide range of cancer cell lines and how coumarins (psoralidin and esculetin) isolated from natural sources have improved TRAIL induced apoptosis in resistant cancer cells. We summarize recent updates on piperlongumine, phenethyl isothiocyanate and luteolin induced activation of TRAIL mediated apoptosis. The data obtained from pre-clinical studies will be helpful in translation of information from benchtop to the bedside.

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“…111 Phenethyl isothiocyanate is an effective constituent obtained from plants from the Brassicaceae family. 112 Its chemopreventive potential against breast cancer cells 113,114 and cervical cancer 115 was investigated previously. Phenethyl isothiocyanate was found to have an apoptosis induction effect in chemotherapeutic drug-resistant cell lines.…”

Section: 73mentioning

confidence: 99%

“…Phenethyl isothiocyanate enhanced death receptor (DR)4 and DR5 and cleaved caspase-3 expression, induced caspase-8, and supressed ERK1/2 and MEK phosphorylation in cervical cancer cells. 7,115 Phenethyl isothiocyanate was also reported to exert an inhibitory effect on the adhesion and invasion of HeLa cells by G2/M phase arrest induction and CDK1, MMP2/9, CD44, intercellular adhesion molecule 1 supression. It was considered to act via the transforming growth factor (TGF)β/Smad2 pathway, evident by increasing TGFβ, IL6, and IL8 production and Smad2 phosphorylation.…”

Section: 73mentioning

confidence: 99%

The Role of Secondary Metabolites on Gynecologic Cancer Therapy: Some Pathways and Mechanisms

Demırel¹,

Süntar²

2017

tjps

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ÖZJinekolojik kanserler insanlarda ve hayvanlarda en yaygın görülen kanserler arasındadır. Tedavi başarısı tanıdaki evre, tümör tipi, orijini ve metastazı içeren birçok faktöre bağlıdır. Günümüzde bu kanserlerin tedavisinde, cerrahi müdahale, kemoterapi ve radyoterapi uygulanmaktadır. Ancak, birçok anti-karsinojenik ilaç ciddi yan etkilere neden olabilir ve ayrıca tedaviye beklenen yanıt alınamayabilir. Son yıllarda yapılan çalışmalarda kanser ve inflamasyon arasındaki ilişkinin önemi vurgulanmıştır. Ve bununla birlikte, inflamatuvar yolaklara karşı yararlı biyoaktif etkiler gösteren birçok fitokimyasalın jinekolojik kanser tedavisi için antikarsinojenik potansiyele sahip olduğu kanıtlanmıştır. Bu derlemede, jinekolojik kanserlerdeki inflamatuvar yolaklar ve bu yolaklarda etkili sekonder metabolitlerin tedavideki rolü özetlenmektedir. Anahtar kelimeler: Jinekolojik kanserler, yolak, sekonder metabolitler, bitkisel bileşenler, inflamasyon Gynecologic cancers are among the most common cancers in humans and animals. Treatment success depends on several factors including stage at diagnosis, tumor type, origin and metastasis. Currently, surgery, chemotherapy, and radiotherapy are preferred in the treatment of these cancers. However, many anticarcinogenic drugs can cause severe adverse effects and also the expected response to treatment may not be obtained. In recent studies, the importance of the relationship between cancer and inflammation has been emphasized. Therefore, several phytochemicals that exhibit beneficial bioactive effects towards inflammatory pathways were proven to have anticarcinogenic potential for gynecologic cancer therapy. This review summarizes the role of inflammatory pathways in gynecologic cancers and effective secondary metabolites for cancer therapy.

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Effect of β-Phenylethyl Isothiocyanate from Cruciferous Vegetables on Growth Inhibition and Apoptosis of Cervical Cancer Cells through the Induction of Death Receptors 4 and 5

Cited by 42 publications

References 43 publications

Phenethyl isothiocyanate inhibits growth of human chronic myeloid leukemia K562 cells via reactive oxygen species generation and caspases

Phenethyl isothiocyanate inhibits growth of human chronic myeloid leukemia K562 cells via reactive oxygen species generation and caspases

Dealing Naturally with Stumbling Blocks on Highways and Byways of TRAIL Induced Signaling

The Role of Secondary Metabolites on Gynecologic Cancer Therapy: Some Pathways and Mechanisms

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