Activation of mPTP-dependent mitochondrial apoptosis pathway by a novel pan HDAC inhibitor resminostat in hepatocellular carcinoma cells

Biochemical and Biophysical Research Communications

Volumn 477, Issue 4, 2016, Pages 527-533

  Fu, Meili ^a   Shi, Wenhong ^b   Li, Zhengling ^c   Liu, Haiyan ^a  

^a LINYI PEOPLE'S HOSPITAL   (China)

^b LINYI CANCER HOSPITAL   (China)

^c TENGZHOU CENTRAL PEOPLE S HOSPITAL   (China)

Author keywords

HDAC inhibitor; Hepatocellular carcinoma (HCC); Mitochondrial apoptosis pathway; mPTP; Resminostat; Sorafenib

Indexed keywords

ADENINE NUCLEOTIDE TRANSLOCASE; CASPASE 9; CASPASE 9 INHIBITOR; CYCLOPHILIN D; CYCLOSPORIN A; CYTOCHROME C; MITOCHONDRIAL PERMEABILITY TRANSITION PORE; RESMINOSTAT; SANGLIFEHRIN A; SHORT HAIRPIN RNA; SORAFENIB; CARRIER PROTEIN; HISTONE DEACETYLASE INHIBITOR; HYDROXAMIC ACID; SULFONAMIDE;

ANTINEOPLASTIC ACTIVITY; ANTIPROLIFERATIVE ACTIVITY; APOPTOSIS; ARTICLE; CANCER PATIENT; CELL ACTIVITY; CONTROLLED STUDY; CYTOTOXICITY; DEPOLARIZATION; ENZYME ACTIVATION; GENE OVEREXPRESSION; HEPG2 CELL LINE; HUMAN; HUMAN CELL; HUMAN TISSUE; LIVER CELL CARCINOMA; MITOCHONDRION; PRIORITY JOURNAL; PROTEIN SECRETION; CELL PROLIFERATION; CELL SURVIVAL; DRUG EFFECTS; LIVER TUMOR; PATHOLOGY; TUMOR CELL LINE;

APOPTOSIS; CARCINOMA, HEPATOCELLULAR; CELL LINE, TUMOR; CELL PROLIFERATION; CELL SURVIVAL; HISTONE DEACETYLASE INHIBITORS; HUMANS; HYDROXAMIC ACIDS; LIVER NEOPLASMS; MITOCHONDRIAL MEMBRANE TRANSPORT PROTEINS; SULFONAMIDES;

EID: 84979658623     PISSN: 0006291X     EISSN: 10902104     Source Type: Journal    
DOI: 10.1016/j.bbrc.2016.04.147     Document Type: Article

References (29)

1. [1] Singh, S., Singh, P.P., Roberts, L.R., Sanchez, W., Chemopreventive strategies in hepatocellular carcinoma. Nat. Rev. Gastroenterol. Hepatol. 11 (2014), 45–54.
2. [2] Llovet, J.M., Bruix, J., Systematic review of randomized trials for unresectable hepatocellular carcinoma: chemoembolization improves survival. Hepatology 37 (2003), 429–442.
3. [3] Fu, M., Wan, F., Li, Z., Zhang, F., 4SC-202 activates ASK1-dependent mitochondrial apoptosis pathway to inhibit hepatocellular carcinoma cells. Biochem. Biophys. Res. Commun. 471 (2016), 267–273.
4. [4] Ozen, C., Yildiz, G., Dagcan, A.T., Cevik, D., Ors, A., Keles, U., Topel, H., Ozturk, M., Genetics and epigenetics of liver cancer. N. Biotechnol. 30 (2013), 381–384.
5. [5] Falkenberg, K.J., Johnstone, R.W., Histone deacetylases and their inhibitors in cancer, neurological diseases and immune disorders. Nat. Rev. Drug Discov. 13 (2014), 673–691.
6. [6] Marks, P., Rifkind, R.A., Richon, V.M., Breslow, R., Miller, T., Kelly, W.K., Histone deacetylases and cancer: causes and therapies. Nat. Rev. Cancer 1 (2001), 194–202.
7. [7] Hojfeldt, J.W., Agger, K., Helin, K., Histone lysine demethylases as targets for anticancer therapy. Nat. Rev. Drug Discov. 12 (2013), 917–930.
8. [8] Witt, O., Deubzer, H.E., Milde, T., Oehme, I., HDAC family: what are the cancer relevant targets?. Cancer Lett. 277 (2009), 8–21.
9. [9] Weichert, W., HDAC expression and clinical prognosis in human malignancies. Cancer Lett. 280 (2009), 168–176.
10. [10] Bitzer, M., Horger, M., Giannini, E.G., Ganten, T.M., Worns, M.A., Siveke, J.T., Dollinger, M.M., Gerken, G., Scheulen, M.E., Wege, H., Zagonel, V., Cillo, U., Trevisani, F., Santoro, A., Montesarchio, V., Malek, N.P., Holzapfel, J., Herz, T., Ammendola, A.S., Pegoraro, S., Hauns, B., Mais, A., Lauer, U.M., Henning, S.W., Hentsch, B., Resminostat in combination with sorafenib as second-line therapy of advanced hepatocellular carcinoma – the SHELTER Study. J. Hepatol., 2016.
11. [11] Halestrap, A.P., McStay, G.P., Clarke, S.J., The permeability transition pore complex: another view. Biochimie 84 (2002), 153–166.
12. [12] Maes, T., Carceller, E., Salas, J., Ortega, A., Buesa, C., Advances in the development of histone lysine demethylase inhibitors. Curr. Opin. Pharmacol. 23 (2015), 52–60.
13. [13] Li, J., Liu, P., Zhang, R., Cao, L., Qian, H., Liao, J., Xu, W., Wu, M., Yin, Z., Icaritin induces cell death in activated hepatic stellate cells through mitochondrial activated apoptosis and ameliorates the development of liver fibrosis in rats. J. Ethnopharmacol. 137 (2011), 714–723.
14. [14] Zhang, Y.M., Zhang, Z.Q., Liu, Y.Y., Zhou, X., Shi, X.H., Jiang, Q., Fan, D.L., Cao, C., Requirement of Galphai1/3-Gab1 signaling complex for keratinocyte growth factor-induced PI3K-AKT-mTORC1 activation. J. Investig. Dermatol. 135 (2015), 181–191.
15. [15] Zhu, Y.R., Min, H., Fang, J.F., Zhou, F., Deng, X.W., Zhang, Y.Q., Activity of the novel dual phosphatidylinositol 3-kinase/mammalian target of rapamycin inhibitor NVP-BEZ235 against osteosarcoma. Cancer Biol. Ther. 16 (2015), 602–609.
16. [16] Zheng, K., Sheng, Z., Li, Y., Lu, H., Salidroside inhibits oxygen glucose deprivation (OGD)/re-oxygenation-induced H9c2 cell necrosis through activating of Akt-Nrf2 signaling. Biochem. Biophys. Res. Commun. 451 (2014), 79–85.
17. [17] Zhen, Y.F., Wang, G.D., Zhu, L.Q., Tan, S.P., Zhang, F.Y., Zhou, X.Z., Wang, X.D., P53 dependent mitochondrial permeability transition pore opening is required for dexamethasone-induced death of osteoblasts. J. Cell Physiol., 2014.
18. [18] Qiu, Y., Yu, T., Wang, W., Pan, K., Shi, D., Sun, H., Curcumin-induced melanoma cell death is associated with mitochondrial permeability transition pore (mPTP) opening. Biochem. Biophys. Res. Commun. 448 (2014), 15–21.
19. [19] Zhen, Y.F., Wang, G.D., Zhu, L.Q., Tan, S.P., Zhang, F.Y., Zhou, X.Z., Wang, X.D., P53 dependent mitochondrial permeability transition pore opening is required for dexamethasone-induced death of osteoblasts. J. Cell Physiol. 229 (2014), 1475–1483.
20. [20] Yu, T., Chen, C., Sun, Y., Sun, H., Li, T.H., Meng, J., Shi, X., ABT-737 sensitizes curcumin-induced anti-melanoma cell activity through facilitating mPTP death pathway. Biochem. Biophys. Res. Commun. 464 (2015), 286–291.
21. [21] Zhou, C., Chen, Z., Lu, X., Wu, H., Yang, Q., Xu, D., Icaritin activates JNK-dependent mPTP necrosis pathway in colorectal cancer cells. Tumour Biol., 2015.
22. [22] Clarke, S.J., McStay, G.P., Halestrap, A.P., Sanglifehrin A acts as a potent inhibitor of the mitochondrial permeability transition and reperfusion injury of the heart by binding to cyclophilin-D at a different site from cyclosporin A. J. Biol. Chem. 277 (2002), 34793–34799.
23. [23] Uchino, H., Ishii, N., Shibasaki, F., Calcineurin and cyclophilin D are differential targets of neuroprotection by immunosuppressants CsA and FK506 in ischemic brain damage. Acta Neurochir. Suppl. 86 (2003), 105–111.
24. [24] Tanaka, S., Arii, S., Molecular targeted therapies in hepatocellular carcinoma. Semin. Oncol. 39 (2012), 486–492.
25. [25] Wu, L.M., Yang, Z., Zhou, L., Zhang, F., Xie, H.Y., Feng, X.W., Wu, J., Zheng, S.S., Identification of histone deacetylase 3 as a biomarker for tumor recurrence following liver transplantation in HBV-associated hepatocellular carcinoma. PLoS One, 5, 2010, e14460.
26. [26] Rikimaru, T., Taketomi, A., Yamashita, Y., Shirabe, K., Hamatsu, T., Shimada, M., Maehara, Y., Clinical significance of histone deacetylase 1 expression in patients with hepatocellular carcinoma. Oncology 72 (2007), 69–74.
27. [27] Anestopoulos, I., Voulgaridou, G.P., Georgakilas, A.G., Franco, R., Pappa, A., Panayiotidis, M.I., Epigenetic therapy as a novel approach in hepatocellular carcinoma. Pharmacol. Ther. 145 (2015), 103–119.
28. [28] Coradini, D., Speranza, A., Histone deacetylase inhibitors for treatment of hepatocellular carcinoma. Acta Pharmacol. Sin. 26 (2005), 1025–1033.
29. [29] Escudier, B., Eisen, T., Stadler, W.M., Szczylik, C., Oudard, S., Siebels, M., Negrier, S., Chevreau, C., Solska, E., Desai, A.A., Rolland, F., Demkow, T., Hutson, T.E., Gore, M., Freeman, S., Schwartz, B., Shan, M., Simantov, R., Bukowski, R.M., Sorafenib in advanced clear-cell renal-cell carcinoma. N. Engl. J. Med. 356 (2007), 125–134.