|
1
|
Roberti A, La Sala D and Cinti C: Multiple
genetic and epigenetic interacting mechanisms contribute to
clonally selection of drug-resistant tumors: current views and new
therapeutic prospective. J Cell Physiol. 207:571–581. 2006.
View Article : Google Scholar
|
|
2
|
Glasspool RM, Teodoridis JM and Brown R:
Epigenetics as a mechanism driving polygenic clinical drug
resistance. Br J Cancer. 94:1087–1092. 2006. View Article : Google Scholar : PubMed/NCBI
|
|
3
|
Iwasa Y, Nowak MA and Michor F: Evolution
of resistance during clonal expansion. Genetics. 172:2557–2566.
2006. View Article : Google Scholar : PubMed/NCBI
|
|
4
|
Bartel DP: MicroRNAs: genomics,
biogenesis, mechanism, and function. Cell. 116:281–297. 2004.
View Article : Google Scholar : PubMed/NCBI
|
|
5
|
Slaby O, Jancovicova J, Lakomy R, et al:
Expression of miRNA-106b in conventional renal cell carcinoma is a
potential marker for prediction of early metastasis after
nephrectomy. J Exp Clin Cancer Res. 29:902010. View Article : Google Scholar : PubMed/NCBI
|
|
6
|
Philippidou D, Schmitt M, Moser D, et al:
Signatures of microRNAs and selected microRNA target genes in human
melanoma. Cancer Res. 70:4163–4173. 2010. View Article : Google Scholar : PubMed/NCBI
|
|
7
|
Karakatsanis A, Papaconstantinou I,
Gazouli M, Lyberopoulou A, Polymeneas G and Voros D: Expression of
microRNAs, miR-21, miR-31, miR-122, miR-145, miR-146a, miR-200c,
miR-221, miR-222, and miR-223 in patients with hepatocellular
carcinoma or intrahepatic cholangiocarcinoma and its prognostic
significance. Mol Carcinog. Dec 27–2011.(Epub ahead of print).
View Article : Google Scholar
|
|
8
|
Cochrane DR, Spoelstra NS, Howe EN,
Nordeen SK and Richer JK: MicroRNA-200c mitigates invasiveness and
restores sensitivity to microtubule-targeting chemotherapeutic
agents. Mol Cancer Ther. 8:1055–1066. 2009. View Article : Google Scholar : PubMed/NCBI
|
|
9
|
Ceppi P, Mudduluru G, Kumarswamy R, et al:
Loss of miR-200c expression induces an aggressive, invasive, and
chemoresistant phenotype in non-small cell lung cancer. Mol Cancer
Res. 8:1207–1216. 2010. View Article : Google Scholar : PubMed/NCBI
|
|
10
|
Kovalchuk O, Filkowski J, Meservy J, et
al: Involvement of microRNA-451 in resistance of the MCF-7 breast
cancer cells to chemotherapeutic drug doxorubicin. Mol Cancer Ther.
7:2152–2159. 2008. View Article : Google Scholar : PubMed/NCBI
|
|
11
|
Li Z, Wang L, Zhang W, et al: Restoring
E-cadherin-mediated cell-cell adhesion increases PTEN protein level
and stability in human breast carcinoma cells. Biochem Biophys Res
Commun. 363:165–170. 2007. View Article : Google Scholar : PubMed/NCBI
|
|
12
|
Kim SM, Kim JS, Kim JH, et al: Acquired
resistance to cetuximab is mediated by increased PTEN instability
and leads cross-resistance to gefitinib in HCC827 NSCLC cells.
Cancer Lett. 296:150–159. 2010. View Article : Google Scholar : PubMed/NCBI
|
|
13
|
Park SM, Gaur AB, Lengyel E and Peter ME:
The miR-200 family determines the epithelial phenotype of cancer
cells by targeting the E-cadherin repressors ZEB1 and ZEB2. Genes
Dev. 22:894–907. 2008. View Article : Google Scholar : PubMed/NCBI
|
|
14
|
Lau MT, Klausen C and Leung PC: E-cadherin
inhibits tumor cell growth by suppressing PI3K/Akt signaling via
β-catenin-Egr1-mediated PTEN expression. Oncogene. 30:2753–2766.
2011.PubMed/NCBI
|
|
15
|
Selga E, Morales C, Noé V, Peinado MA and
Ciudad CJ: Role of caveolin 1, E-cadherin, Enolase 2 and PKCalpha
on resistance to methotrexate in human HT29 colon cancer cells. BMC
Med Genomics. 1:352008. View Article : Google Scholar : PubMed/NCBI
|
|
16
|
Hurteau GJ, Carlson JA, Spivack SD and
Brock GJ: Overexpression of the microRNA hsa-miR-200c leads to
reduced expression of transcription factor 8 and increased
expression of E-cadherin. Cancer Res. 67:7972–7976. 2007.
View Article : Google Scholar : PubMed/NCBI
|
|
17
|
Eger A, Aigner K, Sonderegger S, et al:
DeltaEF1 is a transcriptional repressor of E-cadherin and regulates
epithelial plasticity in breast cancer cells. Oncogene.
24:2375–2385. 2005. View Article : Google Scholar : PubMed/NCBI
|
|
18
|
Tryndyak VP, Beland FA and Pogribny IP:
E-cadherin transcriptional down-regulation by epigenetic and
microRNA-200 family alterations is related to mesenchymal and
drug-resistant phenotypes in human breast cancer cells. Int J
Cancer. 126:2575–2583. 2010.
|
|
19
|
Hurteau GJ, Spivack SD and Brock GJ:
Potential mRNA degradation targets of hsa-miR-200c, identified
using informatics and qRT-PCR. Cell Cycle. 5:1951–1956. 2006.
View Article : Google Scholar : PubMed/NCBI
|
|
20
|
Junxia W, Ping G, Yuan H, et al: Double
strand RNA-guided endogeneous E-cadherin up-regulation induces the
apoptosis and inhibits proliferation of breast carcinoma cells in
vitro and in vivo. Cancer Sci. 101:1790–1796. 2010. View Article : Google Scholar : PubMed/NCBI
|
|
21
|
Sasaki CY, Lin HC and Passaniti A:
Expression of E-cadherin reduces bcl-2 expression and increases
sensitivity to etoposide-induced apoptosis. Int J Cancer.
86:660–666. 2000. View Article : Google Scholar : PubMed/NCBI
|
|
22
|
Ferreira P, Oliveira MJ, Beraldi E, et al:
Loss of functional E-cadherin renders cells more resistant to the
apoptotic agent taxol in vitro. Exp Cell Res. 310:99–104. 2005.
View Article : Google Scholar : PubMed/NCBI
|
|
23
|
Black PC, Brown GA, Inamoto T, et al:
Sensitivity to epidermal growth factor receptor inhibitor requires
E-cadherin expression in urothelial carcinoma cells. Clin Cancer
Res. 14:1478–1486. 2008. View Article : Google Scholar : PubMed/NCBI
|
|
24
|
Witta SE, Gemmill RM, Hirsch FR, et al:
Restoring E-cadherin expression increases sensitivity to epidermal
growth factor receptor inhibitors in lung cancer cell lines. Cancer
Res. 66:944–950. 2006. View Article : Google Scholar : PubMed/NCBI
|
|
25
|
Vivanco I and Sawyers CL: The
phosphatidylinositol 3-kinase AKT pathway in human cancer. Nat Rev
Cancer. 2:489–501. 2002. View
Article : Google Scholar : PubMed/NCBI
|
|
26
|
Oki E, Baba H, Tokunaga E, et al: Akt
phosphorylation associates with LOH of PTEN and leads to
chemoresistance for gastric cancer. Int J Cancer. 117:376–380.
2005. View Article : Google Scholar : PubMed/NCBI
|
|
27
|
Stassi G, Garofalo M, Zerilli M, et al:
PED mediates AKT-dependent chemoresistance in human breast cancer
cells. Cancer Res. 65:6668–6675. 2005. View Article : Google Scholar : PubMed/NCBI
|
|
28
|
Myers MP, Pass I, Batty IH, et al: The
lipid phosphatase activity of PTEN is critical for its tumor
supressor function. Proc Natl Acad Sci USA. 95:13513–13518. 1998.
View Article : Google Scholar : PubMed/NCBI
|
|
29
|
Lee S, Choi EJ, Jin C and Kim DH:
Activation of PI3K/Akt pathway by PTEN reduction and PIK3CA mRNA
amplification contributes to cisplatin resistance in an ovarian
cancer cell line. Gynecol Oncol. 97:26–34. 2005. View Article : Google Scholar : PubMed/NCBI
|
