6-C-(E-phenylethenyl)naringenin induces cell growth inhibition and cytoprotective autophagy in colon cancer cells

European Journal of Cancer

Volumn 68, Issue , 2016, Pages 38-50

  Zhao, Yueliang ^a   Fan, Daming ^a   Ru, Beibei ^a   Cheng, Ka Wing ^b   Hu, Shuting ^a   Zhang, Jiangwen ^a   Li, Edmund T S ^a   Wang, Mingfu ^a  

^a UNIVERSITY OF HONG KONG   (Hong Kong)

^b PEKING UNIVERSITY   (China)

Author keywords

6 CEPN; Anticancer; Colon cancer; RAS

Indexed keywords

6 C (PHENYLETHENYL)NARINGENIN; ANTINEOPLASTIC AGENT; BECLIN 1; CYCLIN D1; CYTOPROTECTIVE AGENT; CYTOTOXIC AGENT; HIGH MOBILITY GROUP B1 PROTEIN; MAMMALIAN TARGET OF RAPAMYCIN; MITOGEN ACTIVATED PROTEIN KINASE 1; MITOGEN ACTIVATED PROTEIN KINASE 3; MITOGEN ACTIVATED PROTEIN KINASE KINASE; NARINGENIN; NICOTINAMIDE ADENINE DINUCLEOTIDE ADENOSINE DIPHOSPHATE RIBOSYLTRANSFERASE; PHOSPHATIDYLINOSITOL 3 KINASE; PROTEIN KINASE B; PROTEIN S ISOPRENYLCYSTEINE O METHYLTRANSFERASE; RAF PROTEIN; RAS PROTEIN; RETINOBLASTOMA PROTEIN; SALIRASIB; UNCLASSIFIED DRUG; 6-C-(PHENYLETHENYL)NARINGENIN; ATG7 PROTEIN, HUMAN; AUTOPHAGY RELATED PROTEIN 7; BECN1 PROTEIN, HUMAN; ENZYME INHIBITOR; FARNESOL; FLAVANONE DERIVATIVE; MITOGEN ACTIVATED PROTEIN KINASE; PROTEIN METHYLTRANSFERASE; PROTEIN-S-ISOPRENYLCYSTEINE O-METHYLTRANSFERASE; SALICYLIC ACID DERIVATIVE; TARGET OF RAPAMYCIN KINASE;

ANTIPROLIFERATIVE ACTIVITY; ARTICLE; AUTOLYSOSOME; AUTOPHAGOSOME; AUTOPHAGY; CANCER INHIBITION; CELL GROWTH; CELL NUCLEUS; CELL PROLIFERATION; CELL VIABILITY; COLON CANCER; CONCENTRATION RESPONSE; CONTROLLED STUDY; CYTOPLASM; CYTOTOXICITY; DRUG MECHANISM; DRUG PROTEIN BINDING; ENZYME ACTIVATION; ENZYME ACTIVE SITE; G1 PHASE CELL CYCLE CHECKPOINT; GENE EXPRESSION; GENE EXPRESSION PROFILING; GENE SILENCING; GENOME-WIDE ASSOCIATION STUDY; HCT116 CELL LINE; HIGH THROUGHPUT SEQUENCING; HUMAN; HUMAN CELL; MOLECULAR DOCKING; PRIORITY JOURNAL; PROTEIN CLEAVAGE; PROTEIN PHOSPHORYLATION; RNA SEQUENCE; SIGNAL TRANSDUCTION; TREATMENT RESPONSE; ANALOGS AND DERIVATIVES; ANTAGONISTS AND INHIBITORS; CELL SURVIVAL; COLORECTAL TUMOR; DRUG EFFECTS; GENE EXPRESSION REGULATION; GENETICS; HCT 116 CELL LINE; HT-29 CELL LINE; METABOLISM; NECROSIS; TUMOR CELL LINE;

AUTOPHAGY; AUTOPHAGY-RELATED PROTEIN 7; BECLIN-1; CELL LINE, TUMOR; CELL PROLIFERATION; CELL SURVIVAL; COLORECTAL NEOPLASMS; ENZYME INHIBITORS; FARNESOL; FLAVANONES; G1 PHASE CELL CYCLE CHECKPOINTS; GENE EXPRESSION REGULATION, NEOPLASTIC; GENE KNOCKDOWN TECHNIQUES; HCT116 CELLS; HT29 CELLS; HUMANS; MITOGEN-ACTIVATED PROTEIN KINASE KINASES; MITOGEN-ACTIVATED PROTEIN KINASES; MOLECULAR DOCKING SIMULATION; NECROSIS; PHOSPHATIDYLINOSITOL 3-KINASES; PROTEIN METHYLTRANSFERASES; PROTO-ONCOGENE PROTEINS C-AKT; PROTO-ONCOGENE PROTEINS C-RAF; RAS PROTEINS; SALICYLATES; TOR SERINE-THREONINE KINASES;

EID: 84989361085     PISSN: 09598049     EISSN: 18790852     Source Type: Journal    
DOI: 10.1016/j.ejca.2016.09.001     Document Type: Article

References (37)

1. [1] Bournet, B., Buscail, C., Muscari, F., Cordelier, P., Buscail, L., Targeting KRAS for diagnosis, prognosis, and treatment of pancreatic cancer: hopes and realities. Eur J Cancer 54 (2016), 75–83.
2. [2] Downward, J., Targeting RAS signalling pathways in cancer therapy. Nat Rev Cancer 3 (2003), 11–22.
3. [3] Chapnick, D.A., Warner, L., Bernet, J., Rao, T., Liu, X., Partners in crime: the TGFβ and MAPK pathways in cancer progression. Cell Biosci, 1, 2011, 42.
4. [4] Schmukler, E., Kloog, Y., Pinkas-Kramarski, R., Ras and autophagy in cancer development and therapy. Oncotarget 5 (2014), 577–586.
5. [5] Blum, R., Elkon, R., Yaari, S., Zundelevich, A., Jacob-Hirsch, J., Rechavi, G., et al. Gene expression signature of human cancer cell lines treated with the ras inhibitor salirasib (S-farnesylthiosalicylic acid). Cancer Res 67 (2007), 3320–3328.
6. [6] Baines, A.T., Xu, D., Der, C.J., Inhibition of Ras for cancer treatment: the search continues. Future Med Chem 3 (2011), 1787–1808.
7. [7] Spiegel, J., Cromm, P.M., Zimmermann, G., Grossmann, T.N., Waldmann, H., Small-molecule modulation of Ras signaling. Nat Chem Biol 10 (2014), 613–622.
8. [8] Wang, M., Tan, W., Zhou, J., Leow, J., Go, M., Lee, H.S., et al. A small molecule inhibitor of isoprenylcysteine carboxymethyltransferase induces autophagic cell death in PC3 prostate cancer cells. J Biol Chem 283 (2008), 18678–18684.
9. [9] Wang, M., Hossain, M.S., Tan, W., Coolman, B., Zhou, J., Liu, S., et al. Inhibition of isoprenylcysteine carboxylmethyltransferase induces autophagic-dependent apoptosis and impairs tumor growth. Oncogene 29 (2010), 4959–4970.
10. [10] Cheng, K.W., Wong, C.C., Cho, C.K., Chu, I.K., Sze, K.H., Lo, C., et al. Trapping of phenylacetaldehyde as a key mechanism responsible for naringenin's inhibitory activity in mutagenic 2-amino-1-methyl-6-phenylimidazo [4, 5-b] pyridine formation. Chem Res Toxicol 21 (2008), 2026–2034.
11. [11] Cheng, K.W., Preventive potential and mechanism of dietary phenolics on the formation of mutagenic heterocyclic amines. [PhD Thesis], 2009, The University of Hong Kong.
12. [12] Liao, Y., Smyth, G.K., Shi, W., The Subread aligner: fast, accurate and scalable read mapping by seed-and-vote. Nucleic Acids Res, 41, 2013 e108–e108.
13. [13] Liao, Y., Smyth, G.K., Shi, W., featureCounts: an efficient general purpose program for assigning sequence reads to genomic features. Bioinformatics 30 (2014), 923–930.
14. [14] Law, C.W., Chen, Y., Shi, W., Smyth, G.K., Voom: precision weights unlock linear model analysis tools for RNA-seq read counts. Genome Biol, 15, 2014, R29.
15. [15] Ritchie, M.E., Phipson, B., Wu, D., Hu, Y., Law, C.W., Shi, W., et al. Limma powers differential expression analyses for RNA-sequencing and microarray studies. Nucleic Acids Res, 2015, gkv007.
16. [16] Shi, W., Liao, Y., Willis, S.N., Taubenheim, N., Inouye, M., Tarlinton, D.M., et al. Transcriptional profiling of mouse B cell terminal differentiation defines a signature for antibody-secreting plasma cells. Nat Immunol 16 (2015), 663–673.
17. [17] Kramer, K., Harrington, E.O., Lu, Q., Bellas, R., Newton, J., Sheahan, K.L., et al. Isoprenylcysteine carboxyl methyltransferase activity modulates endothelial cell apoptosis. Mol Biol Cell 14 (2003), 848–857.
18. [18] Salyan, M.E.K., Pedicord, D.L., Bergeron, L., Mintier, G.A., Hunihan, L., Kuit, K., et al. A general liquid chromatography/mass spectroscopy-based assay for detection and quantitation of methyltransferase activity. Anal Biochem 349 (2006), 112–117.
19. [19] Kanaan, Z., Rai, S.N., Eichenberger, M.R., Roberts, H., Keskey, B., Pan, J., et al. Plasma miR-21: a potential diagnostic marker of colorectal cancer. Ann Surg 256 (2012), 544–551.
20. [20] Zhang, N., Qi, Y., Wadham, C., Wang, L., Warren, A., Di, W., et al. FTY720 induces necrotic cell death and autophagy in ovarian cancer cells: a protective role of autophagy. Autophagy 6 (2010), 1157–1167.
21. [21] Wu, W.K.K., Cho, C.H., Lee, C.W., Wu, Y.C., Yu, L., Li, Z.J., et al. Macroautophagy and ERK phosphorylation counteract the anti-proliferative effect of proteasome inhibitor in gastric cancer cells. Autophagy 6 (2010), 228–238.
22. [22] Cavaliere, V., Lombardo, T., Costantino, S.N., Kornblihtt, L., Alvarez, E.M., Blanco, G.A., Synergism of arsenic trioxide and MG132 in Raji cells attained by targeting BNIP3, autophagy, and mitochondria with low doses of valproic acid and vincristine. Eur J Cancer 50 (2014), 3243–3261.
23. [23] Hashimoto, I., Koizumi, K., Tatematsu, M., Minami, T., Cho, S., Takeno, N., et al. Blocking on the CXCR4/mTOR signalling pathway induces the anti-metastatic properties and autophagic cell death in peritoneal disseminated gastric cancer cells. Eur J Cancer 44 (2008), 1022–1029.
24. [24] Kondo, Y., Kondo, S., Autophagy and cancer therapy. Autophagy 2 (2006), 85–90.
25. [25] Carew, J.S., Nawrocki, S.T., Cleveland, J.L., Modulating autophagy for therapeutic benefit. Autophagy 3 (2007), 464–467.
26. [26] Høyer-Hansen, M., Jäättelä, M., Autophagy: an emerging target for cancer therapy. Autophagy 4 (2008), 574–580.
27. [27] Coffelt, S.B., Kersten, K., Doornebal, C.W., Weiden, J., Vrijland, K., Hau, C.S., et al. IL-17-producing γδ T cells and neutrophils conspire to promote breast cancer metastasis. Nature 522 (2015), 345–348.
28. [28] Bharate, S.B., Singh, B., Vishwakarma, R.A., Modulation of K-Ras signaling by natural products. Curr Med Chem 19 (2012), 2273–2291.
29. [29] Zundelevich, A., Elad-Sfadia, G., Haklai, R., Kloog, Y., Suppression of lung cancer tumor growth in a nude mouse model by the Ras inhibitor salirasib (farnesylthiosalicylic acid). Mol Cancer Ther 6 (2007), 765–1773.
30. [30] Blum, R., Kloog, Y., Tailoring Ras-pathway-inhibitor combinations for cancer therapy. Drug Resist Update 8 (2005), 369–380.
31. [31] Yaari, S., Jacob-Hirsch, J., Amariglio, N., Haklai, R., Rechavi, G., Kloog, Y., Disruption of cooperation between Ras and MycN in human neuroblastoma cells promotes growth arrest. Clin Cancer Res 11 (2005), 4321–4330.
32. [32] Schmukler, E., Grinboim, E., Schokoroy, S., Amir, A., Wolfson, E., Kloog, Y., et al. Ras inhibition enhances autophagy, which partially protects cells from death. Oncotarget 4 (2013), 142–152.
33. [33] Roberts, P.J., Der, C.J., Targeting the Raf-MEK-ERK mitogen-activated protein kinase cascade for the treatment of cancer. Oncogene 26 (2007), 3291–3310.
34. [34] Schreck, R., Rapp, U.R., Raf kinases: oncogenesis and drug discovery. Int J Cancer 119 (2006), 2261–2271.
35. [35] Sawyers, C.L., Will mTOR inhibitors make it as cancer drugs?. Cancer Cell 4 (2003), 343–348.
36. [36] Morishima, N., Changes in nuclear morphology during apoptosis correlate with vimentin cleavage by different caspases located either upstream or downstream of Bcl-2 action. Genes Cells 4 (1999), 401–414.
37. [37] Gao, J., Liao, J., Yang, G.Y., CAAX-box protein, prenylation process and carcinogenesis. Am J Transl Res 1 (2009), 312–325.