Paper - WANFANG MED ONLINE

You Position: Home > Paper

Relationship of PI3K/AKT/mTOR pathway with TKI drug and radiation resistance

( views:267, downloads:140 )

Author:: No author available

Journal Title:: 国际呼吸杂志

Issue:: 22

DOI:: 10.3760/cma.j.issn.1673-436X.2016.22.015

Key Word:: PI3K/AKT/mTOR;肺癌;酪氨酸激酶抑制剂耐药性;放疗抵抗性;PI3K/AKT/mTOR;Lung cancer;Tyrosine kinase inhibitor resistance;Radiation resistance

Abstract： Lung cancer is the leading cause of cancer-related mortality worldwide.Currently, epidermal growth factor receptor and anti-vascular endothelial growth factor receptor have become first-line clinical application.But the lung carcinoma can tend to be resistant of targeted therapies and radiation. The researches have found that PI3K/AKT/mTOR pathway widely exists in many kinds of cancer cells and it plays an important role in the process of cell growth,proliferation and angiogenesis.We find that the pathways is closely associated with tyrosine kinase inhibitor and radiation resistance.The PI3K/AKT inhibitor could reverse the drug resistance of epidermal growth factor receptor-tyrosine kinase inhibitor. The same as the mTOR inhibitor for the radiation sensitivity.These findings may provide basic evidence for PI3K/AKT inhibitor and mTOR inhibitor applied in the treatment of lung cancer.

Reference

[1]郭其森,朱栋元.晚期非小细胞肺癌靶向治疗进展[J].2012,(14).
[2]陆舜,纪文翔,虞永峰.2014版《NCCN非小细胞肺癌临床实践指南》更新解读[J].2015,(5).
[3]Gadgeel,S.M.,Wozniak,A..Preclinical rationale for PI3K/Akt/mTOR pathway inhibitors as therapy for epidermal growth factor receptor inhibitor-resistant non-small-cell lung cancer[J].2013,14(4).
[4]Thomas K, Sin,Fengfeng, Wang,Fei, Meng,etc.Implications of MicroRNAs in the Treatment of Gefitinib-Resistant Non-Small Cell Lung Cancer.[J].2016.
[5]Arunkumar Anandharaj,Senthilkumar Cinghu,Woo-Yoon Park.Rapamycin-mediated mTOR inhibition attenuates survivin and sensitizes glioblastoma cells to radiation therapy[J].2011,(4).
[6]Kholodenko, B.N.,Kolch, W.,Hoek, J.B.,etc.PI3K/Akt-sensitive MEK-independent compensatory circuit of ERK activation in ER-positive PI3K-mutant T47D breast cancer cells[J].2010,22(9).
[7]Alberto M, Martelli,Camilla, Evangelisti,Francesca, Chiarini,etc.The phosphatidylinositol 3-kinase/Akt/mTOR signaling network as a therapeutic target in acute myelogenous leukemia patients.[J].2010,1.
[8]Shannon, Reagan-Shaw,Nihal, Ahmad.RNA interference-mediated depletion of phosphoinositide 3-kinase activates forkhead box class O transcription factors and induces cell cycle arrest and apoptosis in breast carcinoma cells.[J].2006,66(2).
[9]Li W,Zhou C,Ju L,etc.Integrin beta1 over-expression associates with resistance to tyrosine kinase inhibitor gefitinib in non-small cell lung cancer.[J].2010,111(6).
[10]Roos, Wynand Paul,Kuecuek, Pelin,Tomaszowski, Karl-Heinz,etc.Enhanced Histone Deacetylase Activity in Malignant Melanoma Provokes RAD51 and FANCD2-Triggered Drug Resistance[J].2016,76(10).
[11]Maehama T,Dixon JE.The tumor suppressor, PTEN/MMAC1, dephosphorylates the lipid second messenger, phosphatidylinositol 3,4,5-trisphosphate.[J].1998,273(22).
[12]Tu D,Shepherd FA,Johnston D,etc.Erlotinib in previously treated non-small-cell lung cancer.[J].2005,353(2).
[13]Simona Coco,Anna Truini,Angela Alama,etc.Afatinib resistance in non-small cell lung cancer involves the PI3K/AKT and MAPK/ERK signalling pathways and epithelial-to-mesenchymal transition[J].2015,10(3).
[14]QIN-FANG DENG,BO SU,YIN-MIN ZHAO,etc.Integrin β1-mediated acquired gefitinib resistance in non-small cell lung cancer cells occurs via the phosphoinositide 3-kinase-dependent pathway[J].2016,(1).
[15]Sholl, Lynette M.,Aisner, Dara L.,Varella-Garcia, Marileila,etc.Multi-institutional Oncogenic Driver Mutation Analysis in Lung Adenocarcinoma The Lung Cancer Mutation Consortium Experience[J].2015,10(5).
[16]Liang CG,Li M,Xu BZ,etc.PI3-kinase and mitogen-activated protein kinase in cumulus cells mediate EGF-induced meiotic resumption of porcine oocyte.[J].2008,34(4).
[17]C, Eng.The role of PTEN, a phosphatase gene, in inherited and sporadic nonmedullary thyroid tumors.[J].1999,54.
[18]Cristian, Massacesi,Emmanuelle, Di Tomaso,Patrick, Urban,etc.PI3K inhibitors as new cancer therapeutics: implications for clinical trial design.[J].2016.
[19]D J, Marsh,P L, Dahia,V, Coulon,etc.Allelic imbalance, including deletion of PTEN/MMACI, at the Cowden disease locus on 10q22-23, in hamartomas from patients with Cowden syndrome and germline PTEN mutation.[J].1998,21(1).
[20]Bilanges B,Guillermet Guibert J,Graupera M,etc.The emerging mechanisms of isoform-specific PI3K signalling.[J].2010,11(5).
[21]Normanno N,De Luca A.Predictive biomarkers to tyrosine kinase inhibitors for the epidermal growth factor receptor in non-small-cell lung cancer.[J].2010,11(7).
[22]Rowinsky EK.Targeting the molecular target of rapamycin (mTOR).[J].2004,16(6).
[23]Xipell, Enric,Aragon, Tomas,Martinez-Velez, Naiara,etc.Endoplasmic reticulum stress-inducing drugs sensitize glioma cells to temozolomide through downregulation of MGMT, MPG, and Rad51[J].2016,18(8).
[24]Mataki, Hiroko,Seki, Naohiko,Chiyomaru, Takeshi,etc.Tumor-suppressive microRNA-206 as a dual inhibitor of MET and EGFR oncogenic signaling in lung squamous cell carcinoma[J].2015,46(3).
[25]Ushijima, Hiroki,Suzuki, Yoshiyuki,Oike, Takahiro,etc.Radio-sensitization effect of an mTOR inhibitor, temsirolimus, on lung adenocarcinoma A549 cells under normoxic and hypoxic conditions[J].2015,56(4).