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      Molecular targets of luteolin in cancer

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          Abstract

          Many food-derived phytochemical compounds and their derivatives represent a cornucopia of new anticancer compounds. Despite extensive study of luteolin, the literature has no information on the exact mechanisms or molecular targets through which it deters cancer progression. This review discusses existing data on luteolin’s anticancer activities and then offers possible explanations for and molecular targets of its cancer-preventive action. Luteolin prevents tumor development largely by inactivating several signals and transcription pathways essential for cancer cells. This review also offers insights into the molecular mechanisms and targets through which luteolin either prevents cancer or mediates cancer cell death.

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          Luteolin, a flavonoid with potential for cancer prevention and therapy.

          Yong Wen Lin, Ranxin Shi, Xia Wang … (2008)
          Luteolin, 3',4',5,7-tetrahydroxyflavone, is a common flavonoid that exists in many types of plants including fruits, vegetables, and medicinal herbs. Plants rich in luteolin have been used in Chinese traditional medicine for treating various diseases such as hypertension, inflammatory disorders, and cancer. Having multiple biological effects such as anti-inflammation, anti-allergy and anticancer, luteolin functions as either an antioxidant or a pro-oxidant biochemically. The biological effects of luteolin could be functionally related to each other. For instance, the anti-inflammatory activity may be linked to its anticancer property. Luteolin's anticancer property is associated with the induction of apoptosis, and inhibition of cell proliferation, metastasis and angiogenesis. Furthermore, luteolin sensitizes cancer cells to therapeutic-induced cytotoxicity through suppressing cell survival pathways such as phosphatidylinositol 3'-kinase (PI3K)/Akt, nuclear factor kappa B (NF-kappaB), and X-linked inhibitor of apoptosis protein (XIAP), and stimulating apoptosis pathways including those that induce the tumor suppressor p53. These observations suggest that luteolin could be an anticancer agent for various cancers. Furthermore, recent epidemiological studies have attributed a cancer prevention property to luteolin. In this review, we summarize the progress of recent research on luteolin, with a particular focus on its anticancer role and molecular mechanisms underlying this property of luteolin.
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            Flavonoid (myricetin, quercetin, kaempferol, luteolin, and apigenin) content of edible tropical plants.

            Koo Miean, Suhaila Mohamed (2001)
            Studies were conducted on the flavonoids (myricetin, quercetin, kaempferol, luteolin, and apigenin) contents of 62 edible tropical plants. The highest total flavonoids content was in onion leaves (1497.5 mg/kg quercetin, 391.0 mg/kg luteolin, and 832.0 mg/kg kaempferol), followed by Semambu leaves (2041.0 mg/kg), bird chili (1663.0 mg/kg), black tea (1491.0 mg/kg), papaya shoots (1264.0 mg/kg), and guava (1128.5 mg/kg). The major flavonoid in these plant extracts is quercetin, followed by myricetin and kaempferol. Luteolin could be detected only in broccoli (74.5 mg/kg dry weight), green chili (33.0 mg/kg), bird chili (1035.0 mg/kg), onion leaves (391.0 mg/kg), belimbi fruit (202.0 mg/kg), belimbi leaves (464.5 mg/kg), French bean (11.0 mg/kg), carrot (37.5 mg/kg), white radish (9.0 mg/kg), local celery (80.5 mg/kg), limau purut leaves (30.5 mg/kg), and dried asam gelugur (107.5 mg/kg). Apigenin was found only in Chinese cabbage (187.0 mg/kg), bell pepper (272.0 mg/kg), garlic (217.0 mg/kg), belimbi fruit (458.0 mg/kg), French peas (176.0 mg/kg), snake gourd (42.4 mg/kg), guava (579.0 mg/kg), wolfberry leaves (547.0 mg/kg), local celery (338.5 mg/kg), daun turi (39.5 mg/kg), and kadok (34.5 mg/kg). In vegetables, quercetin glycosides predominate, but glycosides of kaempferol, luteolin, and apigenin are also present. Fruits contain almost exclusively quercetin glycosides, whereas kaempferol and myricetin glycosides are found only in trace quantities.
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              Role of autophagy in cisplatin resistance in ovarian cancer cells.

              Juan Wang, Gen Wu (2014)
              Cisplatin-based treatment is the first line chemotherapy for several cancers including ovarian cancer. The development of cisplatin resistance results in treatment failure, but the underlying mechanisms are not fully understood. Here we show that the induction of autophagy plays an important role in cisplatin resistance in ovarian cancer cells. Specifically, we show that cisplatin resistance is correlated with autophagy induction in a panel of ovarian cancer cells but not in immortalized human ovarian surface epithelial cells. Mechanistically, cisplatin treatment activates ERK and subsequently promotes autophagy. The inhibition of ERK activation with MEK inhibitors or knockdown of ERK expression with siRNA decreases cisplatin-induced autophagy and subsequently sensitizes ovarian cancer cells to cisplatin-induced apoptosis. In ovarian cancer cells that have developed acquired cisplatin resistance, both ERK activation and autophagy induction are increased. Importantly, knockdown of ERK or inhibition of autophagy promotes cisplatin-induced apoptosis in acquired cisplatin-resistant cells. Collectively, our data indicate that ERK-mediated autophagy can lead to cisplatin resistance and suggest that cisplatin resistance can be overcome by inhibition of autophagy in ovarian cancer cells.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Eur J Cancer Prev
                Journal ID (iso-abbrev): Eur. J. Cancer Prev
                Journal ID (publisher-id): CEJ
                Title: European Journal of Cancer Prevention
                Publisher: Lippincott Williams & Wilkins
                ISSN (Print): 0959-8278
                ISSN (Electronic): 1473-5709
                Publication date (Print): January 2016
                Publication date (Electronic): 02 December 2015
                Volume: 25
                Issue: 1
                Pages: 65-76
                Affiliations
                Zoology Department, Division of Physiology, Faculty of Science, Damanhour University, Damanhour, Egypt
                Author notes
                Correspondence to Muobarak J. Tuorkey, PhD, Zoology Department, Faculty of Science, Damanhour University, 14 El-Gomhoria Street, Damanhour, Al-Behira 22111, Egypt Tel: +20 198 624 037; fax: +20 453 368 757; e-mail: physio_mj_tuorkey@ 123456yahoo.com
                Article
                DOI: 10.1097/CEJ.0000000000000128
                PMC ID: 4885545
                PubMed ID: 25714651
                SO-VID: e94c6b27-7712-497f-8d9f-2c34af452de8
                Copyright © Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
                History
                Date received : 4 August 2014
                Date accepted : 23 December 2014
                Categories
                Subject: Review Article: Carcinogenesis

                Keywords: cell cycle arrest,dna methylation,histone modification,pi3k/akt/mtor pathway,wnt/β-catenin signaling
                Data availability:
                Keywords: cell cycle arrest, dna methylation, histone modification, pi3k/akt/mtor pathway, wnt/β-catenin signaling

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