Phytochemicals and PI3K Inhibitors in Cancer—An Insight

Suvarna, Vasanti; Murahari, Manikanta; Khan, Tabassum; Chaubey, Pramila; Sangave, Preeti C.

doi:10.3389/fphar.2017.00916

Cited by 44 publications

(31 citation statements)

References 181 publications

(195 reference statements)

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“…Overall, scientific data have documented that this type of metabolites exerts an inhibitory effect on a broad range of mammalian tumor cell lines in in vitro and in vivo systems [ 8 , 9 ]. According to the literature, the main mammalian cellular and molecular mechanisms influenced by plant molecules are those that involve the following targets: nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB); protein tyrosine kinases (PTKs); target mitogen-activated protein kinases (MAPKs); cyclooxygenase (COX-2); cyclin-dependent kinases (Cdks); phosphoinositide 3-kinase (PI3K) interactors; activator protein 1 (AP1); and cytoskeleton components [ 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 ].…”

Section: Introductionmentioning

confidence: 99%

Oregano Phytocomplex Induces Programmed Cell Death in Melanoma Lines via Mitochondria and DNA Damage

Nanni

Marco

Sacchetti

et al. 2020

Foods

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Plant secondary metabolites possess chemopreventive and antineoplastic properties, but the lack of information about their exact mechanism of action in mammalian cells hinders the translation of these compounds in suitable therapies. In light of this, firstly, Origanum vulgare L. hydroalcoholic extract was chemically characterized by spectrophotometric and chromatographic analyses; then, the molecular bases underlying its antitumor activity on B16-F10 and A375 melanoma cells were investigated. Oregano extract induced oxidative stress and inhibited melanogenesis and tumor cell proliferation, triggering programmed cell death pathways (both apoptosis and necroptosis) through mitochondria and DNA damage. By contrast, oregano extract was safe on healthy tissues, revealing no cytotoxicity and mutagenicity on C2C12 myoblasts, considered as non-tumor proliferating cell model system, and on Salmonella strains, by the Ames test. All these data provide scientific evidence about the potential application of this food plant as an anticancer agent in in vivo studies and clinical trials.

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Section: Introductionmentioning

confidence: 99%

Oregano Phytocomplex Induces Programmed Cell Death in Melanoma Lines via Mitochondria and DNA Damage

Nanni

Marco

Sacchetti

et al. 2020

Foods

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“…Phytochemicals are secondary plant metabolites and include flavonoids, triterpenoids, phenols, alkaloids, catechols, saponins, and tannins. Phytochemicals have been widely used for many decades in the prevention and treatment of various ailments, and current evidence suggests the use of phytochemicals as an effective treatment for cancer [ 9 ]. Phytochemicals, such as vincristine, taxanes, and camptothecin, which exhibit cytotoxic activities, contribute to the effective treatment of cancer.…”

Section: Introductionmentioning

confidence: 99%

Anti-Tumorigenic Activity of Chrysin from Oroxylum indicum via Non-Genotoxic p53 Activation through the ATM-Chk2 Pathway

et al. 2018

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The p53 tumor suppressor plays critical roles in cell cycle regulation and apoptotic cell death in response to various cellular stresses, thereby preventing cancer development. Therefore, the activation of p53 through small molecules is an attractive therapeutic strategy for the treatment of cancers retaining wild-type p53. We used a library of 700 Myanmar wild plant extracts to identify small molecules that induce p53 transcriptional activity. A cell-based screening method with a p53-responsive luciferase-reporter assay system revealed that an ethanol extract of Oroxylum indicum bark increased p53 transcriptional activity. Chrysin was isolated and identified as the active ingredient in the O. indicum bark extract. A treatment with chrysin increased p53 protein expression and the p53-mediated expression of downstream target genes, and decreased cell viability in MCF7 cells, but not in p53-knockdown MCF7 cells. We also found that chrysin activated the ATM-Chk2 pathway in the absence of DNA damage. Hence, the inactivation of the ATM-Chk2 pathway suppressed p53 activation induced by chrysin. These results suggest the potential of chrysin as an anti-cancer drug through the activation of p53 without DNA damage.

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“…These data revealed the key functions of circRNA_100269 and the potential mechanisms underlying the growth and metastasis of GC, which provided substantial evidences on the roles of circRNA_100269 in tumourogenesis. At present, inhibition of PI3K/Akt signaling is considered as a potential therapeutic approach in cancer treatment (28)(29)(30)(31)(32)(33). CircRNA_100269/PI3K/Akt axis could be a putative therapeutic target for the treatment of GC.…”

Section: Resultsmentioning

confidence: 99%

Upregulated circRNA_100269 suppresses the growth and metastasis of gastric cancer by inactivating PI3K/Akt signaling pathway

wang

liu

2020

Preprint

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Background: The expression of circRNA_100269 in gastric cancer (GC) tissues and cells, together with its regulatory roles on GC cells were investigated. Methods: The levels of circRNA_100269 in GC and matched para-carcinoma tissues, as well as in human GC cell lines and normal gastric epithelial cells were evaluated using RT-qPCR. The models with overexpression or knockdown of circRNA_100269 were generated using lentiviral vectors. Cell viability was examined using MTT assay; cell migration and invasive activity were determined by wound healing and Transwell assay. Cell cycle arrest and apoptosis were assessed; molecules involved in PI3K/Akt signaling, apoptosis and EMT were evaluated using RT-qPCR and immunoblotting. Tumour growth and expression of relevant proteins were examined in circRNA_100269 knockout mice.Results: The results indicated the expression of circRNA_100269 was dramatically decreased in GC samples compared with para-carcinoma tissues (p<0.05), while the levels of PI3K were notably increased (p<0.05). Moreover, the level of circRNA_100269 was relevant to histology grade and occurrence of metastasis in GC patients (p<0.05), where circRNA_100269 and PI3K was inversely correlated (p<0.05). Additionally, circRNA_100269 was downregulated in GC cells compared with normal gastric epithelial cells. Overexpressed circRNA_100269 remarkably suppressed the proliferation, migration, invasion and EMT of GC cells (p<0.05), induced cell cycle arrest at G0/G1 phase and promoted cell apoptosis (p<0.05). In addition, PI3K/Akt signaling was involved in circRNA_100269-mediated proliferation, migration, invasion, EMT and apoptosis in GC cells (p<0.05). Knockdown of circRNA_100269 also significantly promoted tumor growth in vivo (p<0.05). Conclusions: the data of the present study suggested that the expression level of circRNA_100269 was decreased in GC tissues and cells. In addition, circRNA_100269 inhibited the progression of GC by suppressing PI3K/Akt signaling. Therefore, circRNA_100269/PI3K/Akt axis may be a potential therapeutic target for GC treatment.

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Phytochemicals and PI3K Inhibitors in Cancer—An Insight

Cited by 44 publications

References 181 publications

Oregano Phytocomplex Induces Programmed Cell Death in Melanoma Lines via Mitochondria and DNA Damage

Oregano Phytocomplex Induces Programmed Cell Death in Melanoma Lines via Mitochondria and DNA Damage

Anti-Tumorigenic Activity of Chrysin from Oroxylum indicum via Non-Genotoxic p53 Activation through the ATM-Chk2 Pathway

Upregulated circRNA_100269 suppresses the growth and metastasis of gastric cancer by inactivating PI3K/Akt signaling pathway

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