Sodium Butyrate (NaBu) is regarded as a potential reagent for cancer therapy. In this study, a specific breast cancer cell population that is resistant NaBu treatment was identified. These cells possess cancer stem cell characters, such as the capability of sphere formation in vitro and high tumor incident rate (85%) in mouse model. Forty percent of the NaBu resistant cells express the cancer stem cells marker, the CD133, whereas only 10% intact cells present the CD133 antigen. Furthermore, the endogenous expressing c-MET contributes to the survival of cancer stem cell population from the treatment of NaBu. The CD133+ group also presents a higher level of c-MET. A combination treatment of MET siRNA and NaBu efficiently prohibited the breast cancer progression, and the incident rate of the tumor decrease to 18%. This study may help to develop a new and alternative strategy for breast cancer therapy.
References
[1]
Pulukuri SMK, Gorantla B, Dasari VR, Gondi CS, Rao JS (2010) Epigenetic upregulation of urokinase plasminogen activator promotes the tropism of mesenchymal stem cells for tumor cells. Molecular cancer research : MCR 8: 1074–1083.
[2]
Soldatenkov VA, Prasad S, Voloshin Y, Dritschilo A (1998) Sodium butyrate induces apoptosis and accumulation of ubiquitinated proteins in human breast carcinoma cells. Cell death and differentiation 5: 307–312.
[3]
Easmon J (2002) Copper and iron complexes with antitumour activity. Expert Opinion on Therapeutic Patents 12: 789–818.
[4]
Fotovati A, Abu-Ali S, Kage M, Shirouzu K, Yamana H, et al. (2011) N-myc Downstream-regulated Gene 1 (NDRG1) a Differentiation Marker of Human Breast Cancer. Pathology oncology research 17. pp. 525–533.
[5]
Nohara K, Yokoyama Y, Kano K (2007) The important role of caspase-10 in sodium butyrate-induced apoptosis. The Kobe journal of medical sciences 53: 265–273.
[6]
Tokunou M, Niki T, Eguchi K, Iba S, Tsuda H, et al. (2001) c-MET expression in myofibroblasts: role in autocrine activation and prognostic significance in lung adenocarcinoma. The American journal of pathology 158: 1451–1463.
[7]
Lengyel E, Prechtel D, Resau JH, Gauger K, Welk A, et al. (2005) C-MET overexpression in node-positive breast cancer identifies patients with poor clinical outcome independent of Her2/neu. International journal of cancer Journal international du cancer 113: 678–682.
[8]
Bardelli A (1999) A Peptide Representing the Carboxyl-terminal Tail of the Met Receptor Inhibits Kinase Activity and Invasive Growth. Journal of Biological Chemistry 274: 29274–29281.
[9]
Bu R, Uddin S, Bavi P, Hussain AR, Al-Dayel F, et al. (2010) HGF/c-MET pathway has a prominent role in mediating antiapoptotic signals through AKT in epithelial ovarian carcinoma. Laboratory investigation; a journal of technical methods and pathology 91: 124–137.
[10]
Ratajczak MZ (2005) Cancer stem cells--normal stem cells “Jedi” that went over to the “dark side”. Folia histochemica et cytobiologica/Polish Academy of Sciences, Polish Histochemical and Cytochemical Society 43: 175–181.
[11]
Finkbeiner MR, Astanehe A, To K, Fotovati A, Davies AH, et al. (2009) Profiling YB-1 target genes uncovers a new mechanism for MET receptor regulation in normal and malignant human mammary cells. Oncogene 28: 1421–1431.
[12]
Miyata Y, Kanetake H, Kanda S (2006) Presence of phosphorylated hepatocyte growth factor receptor/c-MET is associated with tumor progression and survival in patients with conventional renal cell carcinoma. Clinical cancer research : an official journal of the American Association for Cancer Research 12: 4876–4881.
[13]
Puri N, Ahmed S, Janamanchi V, Tretiakova M, Zumba O, et al. (2007) c-MET is a potentially new therapeutic target for treatment of human melanoma. Clinical cancer research : an official journal of the American Association for Cancer Research 13: 2246–2253.
[14]
Peruzzi B, Bottaro DP (2006) Targeting the c-MET signaling pathway in cancer. Clinical cancer research : an official journal of the American Association for Cancer Research 12: 3657–3660.
[15]
Chopin V, Toillon R-A, Jouy N, Le Bourhis X (2002) Sodium butyrate induces P53-independent, Fas-mediated apoptosis in MCF-7 human breast cancer cells. British journal of pharmacology 135: 79–86.
[16]
Lallemand F, Courilleau D, Buquet-Fagot C, Atfi A, Montagne MN, et al. (1999) Sodium butyrate induces G2 arrest in the human breast cancer cells MDA-MB-231 and renders them competent for DNA rereplication. Experimental cell research 247: 432–440.
[17]
Matteucci E, Bendinelli P, Desiderio MA (2009) Nuclear localization of active HGF receptor Met in aggressive MDA-MB231 breast carcinoma cells. Carcinogenesis 30: 937–945.
[18]
Hwang-Verslues WW, Kuo W-H, Chang P-H, Pan C-C, Wang H-H, et al. (2009) Multiple lineages of human breast cancer stem/progenitor cells identified by profiling with stem cell markers. PloS one 4: e8377–e8377.
[19]
Vincan E, Leet CS, Reyes NI, Dilley RJ, Thomas RJ, et al. (2000) Sodium butyrate-induced differentiation of human LIM2537 colon cancer cells decreases GSK-3beta activity and increases levels of both membrane-bound and Apc/axin/GSK-3beta complex-associated pools of beta-catenin. Oncology research 12: 193–201.
[20]
Pellizzaro C (2002) Modulation of angiogenesis-related proteins synthesis by sodium butyrate in colon cancer cell line HT29. Carcinogenesis 23: 735–740.
[21]
Pellizzaro C, Coradini D, Daniotti A, Abolafio G, Daidone MG (2001) Modulation of cell cycle-related protein expression by sodium butyrate in human non-small cell lung cancer cell lines. International journal of cancer Journal international du cancer 91: 654–657.
[22]
Grudzien P, Lo S, Albain KS, Robinson P, Rajan P, et al. (2010) Inhibition of Notch Signaling Reduces the Stem-like Population of Breast Cancer Cells and Prevents Mammosphere Formation. Anticancer Res 30: 3853–3867.
[23]
Swiercz JM, Worzfeld T, Offermanns S (2008) ErbB-2 and met reciprocally regulate cellular signaling via plexin-B1. The Journal of biological chemistry 283: 1893–1901.
