|
1
|
Settakorn J, Lekawanvijit S,
Arpornchayanon O, Rangdaeng S, Vanitanakom P, Kongkarnka S,
Cheepsattayakorn R, Ya-In C and Thorner PS: Spectrum of bone tumors
in Chiang Mai University Hospital, Thailand according to WHO
classification 2002: A study of 1,001 cases. J Med Assoc Thai.
89:780–787. 2006.PubMed/NCBI
|
|
2
|
Friebele JC, Peck J, Pan X, Abdel-Rasoul M
and Mayerson JL: Osteosarcoma: A meta-analysis and review of the
literature. Am J Orthop (Belle Mead NJ). 44:547–553. 2015.
|
|
3
|
Whelan JS, Bielack SS, Marina N, Smeland
S, Jovic G, Hook JM, Krailo M, Anninga J, Butterfass-Bahloul T,
Böhling T, et al: EURAMOS collaborators: EURAMOS-1, an
international randomised study for osteosarcoma: Results from
pre-randomisation treatment. Ann Oncol. 26:407–414. 2015.
View Article : Google Scholar
|
|
4
|
Chen X, Bahrami A, Pappo A, Easton J,
Dalton J, Hedlund E, Ellison D, Shurtleff S, Wu G, Wei L, et al St
Jude Children's Research Hospital-Washington University Pediatric
Cancer Genome Project: Recurrent somatic structural variations
contribute to tumorigenesis in pediatric osteosarcoma. Cell Rep.
7:104–112. 2014. View Article : Google Scholar : PubMed/NCBI
|
|
5
|
Botter SM, Neri D and Fuchs B: Recent
advances in osteosarcoma. Curr Opin Pharmacol. 16:15–23. 2014.
View Article : Google Scholar : PubMed/NCBI
|
|
6
|
Chaiyawat P, Pruksakorn D, Phanphaisarn A,
Teeyakasem P, Klangjorhor J and Settakorn J: Expression patterns of
class I histone deacetylases in osteosarcoma: A novel prognostic
marker with potential therapeutic implications. Mod Pathol.
31:264–274. 2018. View Article : Google Scholar :
|
|
7
|
Xie C, Wu B, Chen B, Shi Q, Guo J, Fan Z
and Huang Y: Histone deacetylase inhibitor sodium butyrate
suppresses proliferation and promotes apoptosis in osteosarcoma
cells by regulation of the MDM2-p53 signaling. Onco Targets Ther.
9:4005–4013. 2016. View Article : Google Scholar : PubMed/NCBI
|
|
8
|
Watanabe K, Okamoto K and Yonehara S:
Sensitization of osteo-sarcoma cells to death receptor-mediated
apoptosis by HDAC inhibitors through downregulation of cellular
FLIP. Cell Death Differ. 12:10–18. 2005. View Article : Google Scholar
|
|
9
|
Rao-Bindal K, Koshkina NV, Stewart J and
Kleinerman ES: The histone deacetylase inhibitor, MS-275
(entinostat), downregulates c-FLIP, sensitizes osteosarcoma cells
to FasL, and induces the regression of osteosarcoma lung
metastases. Curr Cancer Drug Targets. 13:411–422. 2013. View Article : Google Scholar : PubMed/NCBI
|
|
10
|
Zhu S, Denman CJ, Cobanoglu ZS, Kiany S,
Lau CC, Gottschalk SM, Hughes DP, Kleinerman ES and Lee DA: The
narrow-spectrum HDAC inhibitor entinostat enhances NKG2D expression
without NK cell toxicity, leading to enhanced recognition of cancer
cells. Pharm Res. 32:779–792. 2015. View Article : Google Scholar
|
|
11
|
Li Y, Liang Q, Wen YQ, Chen LL, Wang LT,
Liu YL, Luo CQ, Liang HZ, Li MT and Li Z: Comparative proteomics
analysis of human osteosarcomas and benign tumor of bone. Cancer
Genet Cytogenet. 198:97–106. 2010. View Article : Google Scholar : PubMed/NCBI
|
|
12
|
Rao UN, Hood BL, Jones-Laughner JM, Sun M
and Conrads TP: Distinct profiles of oxidative stress-related and
matrix proteins in adult bone and soft tissue osteosarcoma and
desmoid tumors: A proteomics study. Hum Pathol. 44:725–733. 2013.
View Article : Google Scholar
|
|
13
|
Einhorn TA and Gerstenfeld LC: Fracture
healing: Mechanisms and interventions. Nat Rev Rheumatol. 11:45–54.
2015. View Article : Google Scholar :
|
|
14
|
Murao H, Yamamoto K, Matsuda S and Akiyama
H: Periosteal cells are a major source of soft callus in bone
fracture. J Bone Miner Metab. 31:390–398. 2013. View Article : Google Scholar : PubMed/NCBI
|
|
15
|
Han W, He W, Yang W, Li J, Yang Z, Lu X,
Qin A and Qian Y: The osteogenic potential of human bone callus.
Sci Rep. 6:363302016. View Article : Google Scholar : PubMed/NCBI
|
|
16
|
Srisomsap C, Sawangareetrakul P,
Subhasitanont P, Panichakul T, Keeratichamroen S, Lirdprapamongkol
K, Chokchaichamnankit D, Sirisinha S and Svasti J: Proteomic
analysis of cholangiocarcinoma cell line. Proteomics. 4:1135–1144.
2004. View Article : Google Scholar : PubMed/NCBI
|
|
17
|
Herosimczyk A, Dejeans N, Sayd T, Ozgo M,
Skrzypczak WF and Mazur A: Plasma proteome analysis: 2D gels and
chips. J Physiol Pharmacol. 57(Suppl 7): 81–93. 2006.
|
|
18
|
Zhang B, Kirov S and Snoddy J: WebGestalt:
An integrated system for exploring gene sets in various biological
contexts. Nucleic Acids Res. 33:W741–W748. 2005. View Article : Google Scholar : PubMed/NCBI
|
|
19
|
Shannon P, Markiel A, Ozier O, Baliga NS,
Wang JT, Ramage D, Amin N, Schwikowski B and Ideker T: Cytoscape: A
software environment for integrated models of biomolecular
interaction networks. Genome Res. 13:2498–2504. 2003. View Article : Google Scholar : PubMed/NCBI
|
|
20
|
Lotia S, Montojo J, Dong Y, Bader GD and
Pico AR: Cytoscape app store. Bioinformatic s. 29:1350–1351. 2013.
View Article : Google Scholar
|
|
21
|
Pruksakorn D, Teeyakasem P, Klangjorhor J,
Chaiyawat P, Settakorn J, Diskul-Na-Ayudthaya P, Chokchaichamnankit
D, Pothacharoen P and Srisomsap C: Overexpression of KH-type
splicing regulatory protein regulates proliferation, migration, and
implantation ability of osteosarcoma. Int J Oncol. 49:903–912.
2016. View Article : Google Scholar : PubMed/NCBI
|
|
22
|
van Schadewijk A, van't Wout EF, Stolk J
and Hiemstra PS: A quantitative method for detection of spliced
X-box binding protein-1 (XBP1) mRNA as a measure of endoplasmic
reticulum (ER) stress. Cell Stress Chaperones. 17:275–279. 2012.
View Article : Google Scholar :
|
|
23
|
Livak KJ and Schmittgen TD: Analysis of
relative gene expression data using real-time quantitative PCR and
the 2(-Delta Delta C(T)) method. Methods. 25:402–408. 2001.
View Article : Google Scholar
|
|
24
|
Schindeler A, McDonald MM, Bokko P and
Little DG: Bone remodeling during fracture repair: The cellular
picture. Semin Cell Dev Biol. 19:459–466. 2008. View Article : Google Scholar : PubMed/NCBI
|
|
25
|
Mörike M, Schulz M, Nerlich A, Koschnik M,
Teller WM, Vetter U and Brenner RE: Expression of osteoblastic
markers in cultured human bone and fracture callus cells. J Mol Med
(Berl). 73:571–575. 1995. View Article : Google Scholar
|
|
26
|
Luo B and Lee AS: The critical roles of
endoplasmic reticulum chaperones and unfolded protein response in
tumorigenesis and anticancer therapies. Oncogene. 32:805–818. 2013.
View Article : Google Scholar
|
|
27
|
Hanahan D and Weinberg RA: Hallmarks of
cancer: The next generation. Cell. 144:646–674. 2011. View Article : Google Scholar : PubMed/NCBI
|
|
28
|
Obacz J, Avril T, Le Reste PJ, Urra H,
Quillien V, Hetz C and Chevet E: Endoplasmic reticulum proteostasis
in glioblastoma-From molecular mechanisms to therapeutic
perspectives. Sci Signal. 10:102017. View Article : Google Scholar
|
|
29
|
Wang M and Kaufman RJ: The impact of the
endoplasmic reticulum protein-folding environment on cancer
development. Nat Rev Cancer. 14:581–597. 2014. View Article : Google Scholar : PubMed/NCBI
|
|
30
|
Dejeans N, Manié S, Hetz C, Bard F, Hupp
T, Agostinis P, Samali A and Chevet E: Addicted to secrete - novel
concepts and targets in cancer therapy. Trends Mol Med. 20:242–250.
2014. View Article : Google Scholar : PubMed/NCBI
|
|
31
|
Ma Y and Hendershot LM: The role of the
unfolded protein response in tumour development: Friend or foe? Nat
Rev Cancer. 4:966–977. 2004. View Article : Google Scholar : PubMed/NCBI
|
|
32
|
Hetz C: The unfolded protein response:
Controlling cell fate decisions under ER stress and beyond. Nat Rev
Mol Cell Biol. 13:89–102. 2012. View Article : Google Scholar : PubMed/NCBI
|
|
33
|
Dufey E, Urra H and Hetz C: ER
proteostasis addiction in cancer biology:. Novel concepts Semin
Cancer Biol. 33:40–47. 2015. View Article : Google Scholar
|
|
34
|
Lee AS: Glucose-regulated proteins in
cancer: Molecular mechanisms and therapeutic potential. Nat Rev
Cancer. 14:263–276. 2014. View Article : Google Scholar : PubMed/NCBI
|
|
35
|
Wang M, Wey S, Zhang Y, Ye R and Lee AS:
Role of the unfolded protein response regulator GRP78/BiP in
development, cancer, and neurological disorders. Antioxid Redox
Signal. 11:2307–2316. 2009. View Article : Google Scholar : PubMed/NCBI
|
|
36
|
Chang SC, Erwin AE and Lee AS:
Glucose-regulated protein (GRP94 and GRP78) genes share common
regulatory domains and are coordinately regulated by common
trans-acting factors. Mol Cell Biol. 9:2153–2162. 1989. View Article : Google Scholar : PubMed/NCBI
|
|
37
|
Yamamoto K, Sato T, Matsui T, Sato M,
Okada T, Yoshida H, Harada A and Mori K: Transcriptional induction
of mammalian ER quality control proteins is mediated by single or
combined action of ATF6alpha and XBP1. Dev Cell. 13:365–376. 2007.
View Article : Google Scholar : PubMed/NCBI
|
|
38
|
Yoshida H, Matsui T, Yamamoto A, Okada T
and Mori K: XBP1 mRNA is induced by ATF6 and spliced by IRE1 in
response to ER stress to produce a highly active transcription
factor. Cell. 107:881–891. 2001. View Article : Google Scholar
|
|
39
|
Luo J, Xia Y, Luo J, Li J, Zhang C, Zhang
H, Ma T, Yang L and Kong L: GRP78 inhibition enhances ATF4-induced
cell death by the deubiquitination and stabilization of CHOP in
human osteosarcoma. Cancer Lett. 410:112–123. 2017. View Article : Google Scholar : PubMed/NCBI
|
|
40
|
Lee K, Tirasophon W, Shen X, Michalak M,
Prywes R, Okada T, Yoshida H, Mori K and Kaufman RJ: IRE1-mediated
unconventional mRNA splicing and S2P-mediated ATF6 cleavage merge
to regulate XBP1 in signaling the unfolded protein response. Genes
Dev. 16:452–466. 2002. View Article : Google Scholar : PubMed/NCBI
|
|
41
|
Lee E, Nichols P, Spicer D, Groshen S, Yu
MC and Lee AS: GRP78 as a novel predictor of responsiveness to
chemotherapy in breast cancer. Cancer Res. 66:7849–7853. 2006.
View Article : Google Scholar : PubMed/NCBI
|
|
42
|
Mhaidat NM, Alzoubi KH, Almomani N and
Khabour OF: Expression of glucose regulated protein 78 (GRP78)
determines colorectal cancer response to chemotherapy. Cancer
Biomark. 15:197–203. 2015. View Article : Google Scholar
|
|
43
|
Gifford JB, Huang W, Zeleniak AE, Hindoyan
A, Wu H, Donahue TR and Hill R: Expression of GRP78, master
regulator of the unfolded protein response, increases
chemoresistance in pancreatic ductal adenocarcinoma. Mol Cancer
Ther. 15:1043–1052. 2016. View Article : Google Scholar : PubMed/NCBI
|
|
44
|
Li W, Wang W, Dong H, Li Y, Li L, Han L,
Han Z, Wang S, Ma D and Wang H: Cisplatin-induced senescence in
ovarian cancer cells is mediated by GRP78. Oncol Rep. 31:2525–2534.
2014. View Article : Google Scholar : PubMed/NCBI
|
|
45
|
Xia YZ, Yang L, Xue GM, Zhang C, Guo C,
Yang YW, Li SS, Zhang LY, Guo QL and Kong LY: Combining GRP78
suppression and MK2206-induced Akt inhibition decreases
doxorubicin-induced P-glycoprotein expression and mitigates
chemoresistance in human osteosarcoma. Oncotarget. 7:56371–56382.
2016. View Article : Google Scholar : PubMed/NCBI
|
|
46
|
Schewe DM and Aguirre-Ghiso JA:
ATF6alpha-Rheb-mTOR signaling promotes survival of dormant tumor
cells in vivo. Proc Natl Acad Sci USA. 105:10519–10524. 2008.
View Article : Google Scholar : PubMed/NCBI
|
|
47
|
Shapovalov Y, Benavidez D, Zuch D and
Eliseev RA: Proteasome inhibition with bortezomib suppresses growth
and induces apoptosis in osteosarcoma. Int J Cancer. 127:67–76.
2010. View Article : Google Scholar
|
|
48
|
Rasche L, Duell J, Castro IC, Dubljevic V,
Chatterjee M, Knop S, Hensel F, Rosenwald A, Einsele H, Topp MS, et
al: GRP78-directed immunotherapy in relapsed or refractory multiple
myeloma - results from a phase 1 trial with the monoclonal
immunoglobulin M antibody PAT-SM6. Haematologica. 100:377–384.
2015. View Article : Google Scholar : PubMed/NCBI
|
