Login Register Cart 0
Generic placeholder image

Recent Patents on Anti-Cancer Drug Discovery

Editor-in-Chief

ISSN (Print): 1574-8928
ISSN (Online): 2212-3970

Back
Journal Home About Journal Editorial Board Journal Insight Current Issue Volumes/Issues
Subscribe
Research Article

Targeted Therapies in Lung Cancers: Current Landscape and Future Prospects

Author(s): Xin Feng, Wenqing Ding, Junhong Ma, Baijun Liu and Hongmei Yuan*

Volume 16, Issue 4, 2021

Published on: 15 June, 2021

Page: [540 - 551] Pages: 12

DOI: 10.2174/1574892816666210615161501

Price: $65

Abstract

Background: Lung cancer is the most common malignant cancer worldwide. Targeted therapies have emerged as a promising treatment strategy for lung cancers.

Objective: To evaluate the current landscape of targets and find promising targets for future new drug discovery for lung cancers, this research identified the science-technology-clinical development pattern and mapped the interaction network of targets.

Methods: Targets for cancers were classified into 3 groups based on a paper published in Nature. We searched for scientific pieces of literature, patent documents and clinical trials of targets in Group 1 and Group 2 for lung cancers. Then, a target-target interaction network of Group 1 was constructed, and the science-technology-clinical (S-T-C) development patterns of targets in Group 1 were identified. Finally, based on the cluster distribution and the development pattern of targets in Group 1, interactions between the targets were employed to predict potential targets in Group 2 for drug development.

Results: The target-target interaction (TTI) network of group 1 resulted in 3 clusters with different developmental stages. The potential targets in Group 2 are divided into 3 ranks. Level-1 is the first priority and level-3 is the last. Level-1 includes 16 targets, such as STAT3, CRKL, and PTPN11, that are mostly involved in signaling transduction pathways. Level-2 and level-3 contain 8 and 6 targets, respectively, related to various biological functions.

Conclusion: This study will provide references for drug development in lung cancers, emphasizing that priorities should be given to targets in Level-1, whose mechanisms are worth further exploration.

Keywords: Lung cancer, targeted therapies, science-technology-clinic, target-target interaction network, progress and prospects, signal transduction, target prediction.

« Previous Next »
[1]
Gu J, Xu S, Huang L, et al. Value of combining serum carcinoembryonic antigen and PET/CT in predicting EGFR mutation in non-small cell lung cancer. J Thorac Dis 2018; 10(2): 723-31.
[http://dx.doi.org/10.21037/jtd.2017.12.143] [PMID: 29607142]
[2]
Um S-W, Kim HK, Kim Y, et al. Bronchial biopsy specimen as a surrogate for DNA methylation analysis in inoperable lung cancer. Clin Epigenetics 2017; 9(1): 131.
[http://dx.doi.org/10.1186/s13148-017-0432-5] [PMID: 29270240]
[3]
Chen DM, Mao KY, Yang L, Jiang HB. Status of anti-lung cancer drug patents applications in China from 2003 to 2012. Recent Pat Anticancer Drug Discov 2014; 9(2): 221-40.
[http://dx.doi.org/10.2174/15748928113086660045] [PMID: 24171822]
[4]
Valentino F, Borra G, Allione P, Rossi L. Emerging targets in advanced non-small-cell lung cancer. Future Oncol 2018; 14(13s): 61-72.
[http://dx.doi.org/10.2217/fon-2018-0099] [PMID: 29989453]
[5]
Bearz A, Cecco S, Francescon S, Re FL, Corona G, Baldo P. Safety profiles and pharmacovigilance considerations for recently patented anticancer drugs: Lung cancer. Recent Pat Anticancer Drug Discov 2019; 14(3): 242-57.
[http://dx.doi.org/10.2174/1574892814666190726124735] [PMID: 31362665]
[6]
Chen H-L, Shen L-J, Wei C-P, Lu H-M, Hsiao F-Y. Decision to adopt medical technology under the National Health Insurance System in Taiwan: Case study of new molecular targeted drugs among non-small cell lung cancer patients. J Eval Clin Pract 2015; 21(5): 808-16.
[http://dx.doi.org/10.1111/jep.12382] [PMID: 26096761]
[7]
Lee CK, Brown C, Gralla RJ, et al. Impact of EGFR inhibitor in non-small cell lung cancer on progression-free and overall survival: A meta-analysis. J Natl Cancer Inst 2013; 105(9): 595-605.
[http://dx.doi.org/10.1093/jnci/djt072] [PMID: 23594426]
[8]
Du J, Li P, Guo Q, Tang X. Measuring the knowledge translation and convergence in pharmaceutical innovation by funding-science-technology-innovation linkages analysis. J Informetrics 2019; 13(1): 132-48.
[http://dx.doi.org/10.1016/j.joi.2018.12.004]
[9]
Behan FM, Iorio F, Picco G, et al. Prioritization of cancer therapeutic targets using CRISPR-Cas9 screens. Nature 2019; 568(7753): 511-6.
[http://dx.doi.org/10.1038/s41586-019-1103-9] [PMID: 30971826]
[10]
Kang T-H, Yeo M-H, Yoo J-S, Kim H-Y, Chung JS. A novel method for functional prediction of proteins from a protein-protein interaction network. J Korean Phys Soc 2009; 54(4): 1716-20.
[http://dx.doi.org/10.3938/jkps.54.1716]
[11]
van Laarhoven T, Nabuurs SB, Marchiori E. Gaussian interaction profile kernels for predicting drug-target interaction. Bioinformatics 2011; 27(21): 3036-43.
[http://dx.doi.org/10.1093/bioinformatics/btr500] [PMID: 21893517]
[12]
von Mering C, Jensen LJ, Kuhn M, et al. STRING 7- recent developments in the integration and prediction of protein interactions. Nucleic Acids Res 2007; 35: D358-62.
[http://dx.doi.org/10.1093/nar/gkl825] [PMID: 17098935]
[13]
Patterson H, Nibbs R, McInnes I, Siebert S. Protein kinase inhibitors in the treatment of inflammatory and autoimmune diseases. Clin Exp Immunol 2014; 176(1): 1-10.
[http://dx.doi.org/10.1111/cei.12248] [PMID: 24313320]
[14]
Lahiry P, Torkamani A, Schork NJ, Hegele RA. Kinase mutations in human disease: Interpreting genotype-phenotype relationships. Nat Rev Genet 2010; 11(1): 60-74.
[http://dx.doi.org/10.1038/nrg2707] [PMID: 20019687]
[15]
Kashyap MK, Abdel-Rahman O. Expression, regulation and targeting of receptor tyrosine kinases in esophageal squamous cell carcinoma. Mol Cancer 2018; 17(1): 54.
[http://dx.doi.org/10.1186/s12943-018-0790-4] [PMID: 29455652]
[16]
Chen W, Jiang J, Wang PP, et al. Identifying hepatocellular carcinoma driver genes by integrative pathway crosstalk and protein interaction network. DNA Cell Biol 2019; 38(10): 1112-24.
[http://dx.doi.org/10.1089/dna.2019.4869] [PMID: 31464520]
[17]
Gately K, Forde L, Cuffe S, et al. High coexpression of both EGFR and IGF1R correlates with poor patient prognosis in resected non-small-cell lung cancer. Clin Lung Cancer 2014; 15(1): 58-66.
[http://dx.doi.org/10.1016/j.cllc.2013.08.005] [PMID: 24210543]
[18]
Cosimo D, Annick G, David H, et al. EGFR inhibitors for the treatment of lung cancer. WO2020254565, 2020.
[19]
Oxnard GR, Binder A, Jänne PA. New targetable oncogenes in non-small-cell lung cancer. J Clin Oncol 2013; 31(8): 1097-104.
[http://dx.doi.org/10.1200/JCO.2012.42.9829] [PMID: 23401445]
[20]
Mary B, Melissa B. Treatment of advanced HER2 expressing cancer. US20200237910, 2020.
[21]
Verlingue L, Hollebecque A, Lacroix L, et al. Human epidermal receptor family inhibitors in patients with ERBB3 mutated cancers: Entering the back door. Eur J Cancer 2018; 92: 1-10.
[http://dx.doi.org/10.1016/j.ejca.2017.12.020] [PMID: 29413684]
[22]
Noto A, De Vitis C, Roscilli G, et al. Combination therapy with anti-ErbB3 monoclonal antibodies and EGFR TKIs potently inhibits non-small cell lung cancer. Oncotarget 2013; 4(8): 1253-65.
[http://dx.doi.org/10.18632/oncotarget.1141] [PMID: 23896512]
[23]
Kimio Y, Kazuhiko N, Kenji H. Method for treating EGFR-TKIs-resistant non-small cell lung cancer by administration of anti- HER3 antibody-drug conjugate. US20200061031, 2020.
[24]
Huang X, Gan G, Wang X, Xu T, Xie W. The HGF-MET axis coordinates liver cancer metabolism and autophagy for chemotherapeutic resistance. Autophagy 2019; 15(7): 1258-79.
[http://dx.doi.org/10.1080/15548627.2019.1580105] [PMID: 30786811]
[25]
Ma PC, Jagadeeswaran R, Jagadeesh S, et al. Functional expression and mutations of c-Met and its therapeutic inhibition with SU11274 and small interfering RNA in non-small cell lung cancer. Cancer Res 2005; 65(4): 1479-88.
[http://dx.doi.org/10.1158/0008-5472.CAN-04-2650] [PMID: 15735036]
[26]
Fang S, Youni Z. Tyrosine kinase inhibitor and application thereof. US10882853, 2019.
[27]
Chen HX, Sharon E. IGF-1R as an anti-cancer target- trials and tribulations. Chin J Cancer 2013; 32(5): 242-52.
[http://dx.doi.org/10.5732/cjc.012.10263] [PMID: 23601239]
[28]
Wang Y, Yin L, Sun X. CircRNA hsa_circ_0002577 accelerates endometrial cancer progression through activating IGF1R/PI3K/Akt pathway. J Exp Clin Cancer Res 2020; 39(1): 169.
[http://dx.doi.org/10.1186/s13046-020-01679-8] [PMID: 32847606]
[29]
Molina-Arcas M, Hancock DC, Sheridan C, Kumar MS, Downward J. Coordinate direct input of both KRAS and IGF1 receptor to activation of PI3 kinase in KRAS-mutant lung cancer. Cancer Discov 2013; 3(5): 548-63.
[http://dx.doi.org/10.1158/2159-8290.CD-12-0446] [PMID: 23454899]
[30]
Ke D, Jian D, Shingpan C, et al. 2-Aminopyrimidine compound and pharmaceutical composition and use thereof. US10059694, 2018.
[31]
Pottier C, Fresnais M, Gilon M, Jérusalem G, Longuespée R, Sounni NE. Tyrosine kinase inhibitors in cancer: Breakthrough and challenges of targeted therapy. Cancers (Basel) 2020; 12(3): 731.
[http://dx.doi.org/10.3390/cancers12030731] [PMID: 32244867]
[32]
Hung M-S, Lung J-H, Lin Y-C, et al. Comparative analysis of two methods for the detection of EGFR mutations in plasma circulating tumor DNA from lung adenocarcinoma patients. Cancers (Basel) 2019; 11(6): 803.
[http://dx.doi.org/10.3390/cancers11060803] [PMID: 31185703]
[33]
Kujtan L, Subramanian J. Epidermal growth factor receptor tyrosine kinase inhibitors for the treatment of non-small cell lung cancer. Expert Rev Anticancer Ther 2019; 19(7): 547-59.
[http://dx.doi.org/10.1080/14737140.2019.1596030] [PMID: 30913927]
[34]
Wu S-G, Shih J-Y. Management of acquired resistance to EGFR TKI-targeted therapy in advanced non-small cell lung cancer. Mol Cancer 2018; 17(1): 38.
[http://dx.doi.org/10.1186/s12943-018-0777-1] [PMID: 29455650]
[35]
Fumarola C, Bonelli MA, Petronini PG, Alfieri RR. Targeting PI3K/AKT/mTOR pathway in non small cell lung cancer. Biochem Pharmacol 2014; 90(3): 197-207.
[http://dx.doi.org/10.1016/j.bcp.2014.05.011] [PMID: 24863259]
[36]
Xie S, Ni J, McFaline-Figueroa JR, et al. Divergent roles of PI3K isoforms in PTEN-deficient glioblastomas. Cell Rep 2020; 32(13): 108196.
[http://dx.doi.org/10.1016/j.celrep.2020.108196] [PMID: 32997991]
[37]
Nisa L, Häfliger P, Poliaková M, et al. PIK3CA hotspot mutations differentially impact responses to MET targeting in MET-driven and non-driven preclinical cancer models. Mol Cancer 2017; 16(1): 93.
[http://dx.doi.org/10.1186/s12943-017-0660-5] [PMID: 28532501]
[38]
Tan AC. Targeting the PI3K/Akt/mTOR pathway in Non-Small Cell Lung Cancer (NSCLC). Thorac Cancer 2020; 11(3): 511-8.
[http://dx.doi.org/10.1111/1759-7714.13328] [PMID: 31989769]
[39]
Rosanna T, Junya Q, Robert S, Ralph AR. Benzimidazole derivatives as PI3 kinase inhibitors. US10660898, 2020.
[40]
Maria ZK, Rony A-F. Compositions for the treatment of cancer and uses thereof. US20180177776, 2018.
[41]
Chung V, McDonough S, Philip PA, et al. Effect of selumetinib and MK-2206 vs. oxaliplatin and fluorouracil in patients with metastatic pancreatic cancer after prior therapy: SWOG S1115 study randomized clinical trial. JAMA Oncol 2017; 3(4): 516-22.
[http://dx.doi.org/10.1001/jamaoncol.2016.5383] [PMID: 27978579]
[42]
Nogova L, Mattonet C, Scheffler M, et al. Sorafenib and everolimus in patients with advanced solid tumors and KRAS-mutated NSCLC: A phase I trial with early pharmacodynamic FDG-PET assessment. Cancer Med 2020; 9(14): 4991-5007.
[http://dx.doi.org/10.1002/cam4.3131] [PMID: 32436621]
[43]
Lapenna S, Giordano A. Cell cycle kinases as therapeutic targets for cancer. Nat Rev Drug Discov 2009; 8(7): 547-66.
[http://dx.doi.org/10.1038/nrd2907] [PMID: 19568282]
[44]
Krystof V, Uldrijan S. Cyclin-dependent kinase inhibitors as anticancer drugs. Curr Drug Targets 2010; 11(3): 291-302.
[http://dx.doi.org/10.2174/138945010790711950] [PMID: 20210754]
[45]
Fassl A, Brain C, Abu-Remaileh M, et al. Increased lysosomal biomass is responsible for the resistance of triple-negative breast cancers to CDK4/6 inhibition. Sci Adv 2020; 6(25): eabb2210.
[http://dx.doi.org/10.1126/sciadv.abb2210] [PMID: 32704543]
[46]
Roskoski R Jr. Cyclin-dependent protein serine/threonine kinase inhibitors as anticancer drugs. Pharmacol Res 2019; 139: 471-88.
[http://dx.doi.org/10.1016/j.phrs.2018.11.035] [PMID: 30508677]
[47]
Poratti M, Marzaro G. Third-generation CDK inhibitors: A review on the synthesis and binding modes of Palbociclib, Ribociclib and Abemaciclib. Eur J Med Chem 2019; 172: 143-53.
[http://dx.doi.org/10.1016/j.ejmech.2019.03.064] [PMID: 30978559]
[48]
Otto T, Sicinski P. Cell cycle proteins as promising targets in cancer therapy. Nat Rev Cancer 2017; 17(2): 93-115.
[http://dx.doi.org/10.1038/nrc.2016.138] [PMID: 28127048]
[49]
Susan M, Iain M, Jordi B. Therapeutic combination of a third generation EGFR tyrosine kinase inhibitor and a cyclin D kinase inhibitor. US20200155566, 2020.
[50]
Kang MH, Reynolds CP. Bcl-2 inhibitors: Targeting mitochondrial apoptotic pathways in cancer therapy. Clin Cancer Res 2009; 15(4): 1126-32.
[http://dx.doi.org/10.1158/1078-0432.CCR-08-0144] [PMID: 19228717]
[51]
Zhang J, Wang S, Wang L, et al. Prognostic value of Bcl-2 expression in patients with non-small-cell lung cancer: A meta-analysis and systemic review. OncoTargets Ther 2015; 8: 3361-9.
[http://dx.doi.org/10.2147/OTT.S89275] [PMID: 26604794]
[52]
Suvarna V, Singh V, Murahari M. Current overview on the clinical update of Bcl-2 anti-apoptotic inhibitors for cancer therapy. Eur J Pharmacol 2019; 862: 172655.
[http://dx.doi.org/10.1016/j.ejphar.2019.172655] [PMID: 31494078]
[53]
Liu Z, Gao W. Synergistic effects of Bcl-2 inhibitors with AZD9291 on overcoming the acquired resistance of AZD9291 in H1975 cells. Arch Toxicol 2020; 94(9): 3125-36.
[http://dx.doi.org/10.1007/s00204-020-02816-0] [PMID: 32577785]
[54]
Henri L, Neil B, Sean L, et al. Therapeutic methods relating to HSP90 inhibitors. US20200253979, 2020.
[55]
Brodie SA, Li G, El-Kommos A, et al. Class I HDACs are mediators of smoke carcinogen-induced stabilization of DNMT1 and serve as promising targets for chemoprevention of lung cancer. Cancer Prev Res (Phila) 2014; 7(3): 351-61.
[http://dx.doi.org/10.1158/1940-6207.CAPR-13-0254] [PMID: 24441677]
[56]
Li Y, Seto E. HDACs and HDAC inhibitors in cancer development and therapy. Cold Spring Harb Perspect Med 2016; 6(10): a026831.
[http://dx.doi.org/10.1101/cshperspect.a026831] [PMID: 27599530]
[57]
Ramalingam SS, Maitland ML, Frankel P, et al. Carboplatin and paclitaxel in combination with either vorinostat or placebo for first-line therapy of advanced non-small-cell lung cancer. J Clin Oncol 2010; 28(1): 56-62.
[http://dx.doi.org/10.1200/JCO.2009.24.9094] [PMID: 19933908]
[58]
Huimei B. Tetradium lactone alcohol used as the histone deacetylase enzyme inhibitor use. CN108283636, 2019.
[59]
Kotoula V, Krikelis D, Karavasilis V, et al. Expression of DNA repair and replication genes in Non-Small Cell Lung Cancer (NSCLC): A role for thymidylate synthetase (TYMS). BMC Cancer 2012; 12(1): 342.
[http://dx.doi.org/10.1186/1471-2407-12-342] [PMID: 22866924]
[60]
Shanshan C, Yan Z, Jiangyue C, Duheng L, Yong R. Primer group, reagent and/or kit, system and application thereof for detecting lung cancer chemotherapy related genes. CN109517900, 2020.
[61]
Tyner JW, Erickson H, Deininger MWN, et al. High-throughput sequencing screen reveals novel, transforming RAS mutations in myeloid leukemia patients. Blood 2009; 113(8): 1749-55.
[http://dx.doi.org/10.1182/blood-2008-04-152157] [PMID: 19075190]
[62]
Plotnik JP, Hollenhorst PC. Interaction with ZMYND11 mediates opposing roles of Ras-responsive transcription factors ETS1 and ETS2. Nucleic Acids Res 2017; 45(8): 4452-62.
[http://dx.doi.org/10.1093/nar/gkx039] [PMID: 28119415]
[63]
Román M, Baraibar I, López I, et al. KRAS oncogene in non-small cell lung cancer: Clinical perspectives on the treatment of an old target. Mol Cancer 2018; 17(1): 33.
[http://dx.doi.org/10.1186/s12943-018-0789-x] [PMID: 29455666]
[64]
Ohashi K, Sequist LV, Arcila ME, et al. Characteristics of lung cancers harboring NRAS mutations. Clin Cancer Res 2013; 19(9): 2584-91.
[http://dx.doi.org/10.1158/1078-0432.CCR-12-3173] [PMID: 23515407]
[65]
Gril B, Vidal M, Assayag F, Poupon M-F, Liu W-Q, Garbay C. Grb2-SH3 ligand inhibits the growth of HER2+ cancer cells and has antitumor effects in human cancer xenografts alone and in combination with docetaxel. Int J Cancer 2007; 121(2): 407-15.
[http://dx.doi.org/10.1002/ijc.22674] [PMID: 17372910]
[66]
Jiang W, Wei K, Pan C, et al. MicroRNA-1258 suppresses tumour progression via GRB2/Ras/Erk pathway in non-small-cell lung cancer. Cell Prolif 2018; 51(6): e12502.
[http://dx.doi.org/10.1111/cpr.12502] [PMID: 30069987]
[67]
Bracht JWP, Karachaliou N, Bivona T, et al. BRAF mutations classes I, II, and III in NSCLC patients included in the SLLIP trial: The need for a new pre-clinical treatment rationale. Cancers (Basel) 2019; 11(9): 1381.
[http://dx.doi.org/10.3390/cancers11091381] [PMID: 31533235]
[68]
Mainardi S, Mulero-Sánchez A, Prahallad A, et al. SHP2 is required for growth of KRAS-mutant non-small-cell lung cancer in vivo. Nat Med 2018; 24(7): 961-7.
[http://dx.doi.org/10.1038/s41591-018-0023-9] [PMID: 29808006]
[69]
Cheung HW, Du J, Boehm JS, et al. Amplification of CRKL induces transformation and epidermal growth factor receptor inhibitor resistance in human non-small cell lung cancers. Cancer Discov 2011; 1(7): 608-25.
[http://dx.doi.org/10.1158/2159-8290.CD-11-0046] [PMID: 22586683]
[70]
Kim YH, Kwei KA, Girard L, et al. Genomic and functional analysis identifies CRKL as an oncogene amplified in lung cancer. Oncogene 2010; 29(10): 1421-30.
[http://dx.doi.org/10.1038/onc.2009.437] [PMID: 19966867]
[71]
Yao G, Tang J, Yang X, et al. Cyclin K interacts with β-catenin to induce Cyclin D1 expression and facilitates tumorigenesis and radioresistance in lung cancer. Theranostics 2020; 10(24): 11144-58.
[http://dx.doi.org/10.7150/thno.42578] [PMID: 33042275]
[72]
Stewart DJ. Wnt signaling pathway in non-small cell lung cancer. JNCI J Natl Cancer Inst 2014; 106(1): djt356.
[73]
Sechler M, Borowicz S, Van Scoyk M, et al. Novel role for γ- catenin in the regulation of cancer cell migration via the induction of hepatocyte growth factor activator inhibitor type 1 (HAI-1). J Biol Chem 2015; 290(25): 15610-20.
[http://dx.doi.org/10.1074/jbc.M114.631820] [PMID: 25925948]
[74]
Winn RA, Bremnes RM, Bemis L, et al. γ-Catenin expression is reduced or absent in a subset of human lung cancers and re-expression inhibits transformed cell growth. Oncogene 2002; 21(49): 7497-506.
[http://dx.doi.org/10.1038/sj.onc.1205963] [PMID: 12386812]
[75]
Gennaro VJ, Stanek TJ, Peck AR, et al. Control of CCND1 ubiquitylation by the catalytic SAGA subunit USP22 is essential for cell cycle progression through G1 in cancer cells. Proc Natl Acad Sci USA 2018; 115(40): E9298-307.
[http://dx.doi.org/10.1073/pnas.1807704115] [PMID: 30224477]
[76]
Ding H, Luo Y, Hu K, Liu P, Xiong M. Linc00467 promotes lung adenocarcinoma proliferation via sponging miR-20b-5p to activate CCND1 expression. OncoTargets Ther 2019; 12: 6733-43.
[http://dx.doi.org/10.2147/OTT.S207748] [PMID: 31686834]
[77]
Zhao X, Xu Z, Wang Z, et al. RNA silencing of integrin-linked kinase increases the sensitivity of the A549 lung cancer cell line to cisplatin and promotes its apoptosis. Mol Med Rep 2015; 12(1): 960-6.
[http://dx.doi.org/10.3892/mmr.2015.3471] [PMID: 25760437]
[78]
Chen BB, Glasser JR, Coon TA, et al. F-box protein FBXL2 targets cyclin D2 for ubiquitination and degradation to inhibit leukemic cell proliferation. Blood 2012; 119(13): 3132-41.
[http://dx.doi.org/10.1182/blood-2011-06-358911] [PMID: 22323446]
[79]
Hung C-S, Wang S-C, Yen Y-T, Lee T-H, Wen W-C, Lin R-K. Hypermethylation of CCND2 in lung and breast cancer is a potential biomarker and drug target. Int J Mol Sci 2018; 19(10): 3096.
[http://dx.doi.org/10.3390/ijms19103096] [PMID: 30308939]
[80]
Liang Y, Zhang D, Li L, et al. Exosomal microRNA-144 from bone marrow-derived mesenchymal stem cells inhibits the progression of non-small cell lung cancer by targeting CCNE1 and CCNE2. Stem Cell Res Ther 2020; 11(1): 87.
[http://dx.doi.org/10.1186/s13287-020-1580-7] [PMID: 32102682]
[81]
Huang LN, Wang DS, Chen YQ, et al. Meta-analysis for cyclin E in lung cancer survival. Clin Chim Acta 2012; 413(7-8): 663-8.
[http://dx.doi.org/10.1016/j.cca.2011.12.020] [PMID: 22244930]
[82]
Blanchard J-M. Cyclin A2 transcriptional regulation: Modulation of cell cycle control at the G1/S transition by peripheral cues. Biochem Pharmacol 2000; 60(8): 1179-84.
[http://dx.doi.org/10.1016/S0006-2952(00)00384-1] [PMID: 11007956]
[83]
Gopinathan L, Tan SLW, Padmakumar VC, Coppola V, Tessarollo L, Kaldis P. Loss of Cdk2 and cyclin A2 impairs cell proliferation and tumorigenesis. Cancer Res 2014; 74(14): 3870-9.
[http://dx.doi.org/10.1158/0008-5472.CAN-13-3440] [PMID: 24802190]
[84]
Yin Z, Zhang Y, Li Y, Lv T, Liu J, Wang X. Prognostic significance of STAT3 expression and its correlation with chemoresistance of non-small cell lung cancer cells. Acta Histochem 2012; 114(2): 151-8.
[http://dx.doi.org/10.1016/j.acthis.2011.04.002] [PMID: 21549414]
[85]
Haura EB, Zheng Z, Song L, Cantor A, Bepler G. Activated epidermal growth factor receptor-Stat-3 signaling promotes tumor survival in vivo in non-small cell lung cancer. Clin Cancer Res 2005; 11(23): 8288-94.
[http://dx.doi.org/10.1158/1078-0432.CCR-05-0827] [PMID: 16322287]
[86]
Jiang R, Jin Z, Liu Z, Sun L, Wang L, Li K. Correlation of activated STAT3 expression with clinicopathologic features in lung adenocarcinoma and squamous cell carcinoma. Mol Diagn Ther 2011; 15(6): 347-52.
[http://dx.doi.org/10.1007/BF03256470] [PMID: 22208386]
[87]
Xu L, Qiu S, Yang L, et al. Aminocyanopyridines as anti-lung cancer agents by inhibiting the STAT3 pathway. Mol Carcinog 2019; 58(8): 1512-25.
[http://dx.doi.org/10.1002/mc.23038] [PMID: 31069881]
[88]
Beebe JD, Liu J-Y, Zhang J-T. Two decades of research in discovery of anticancer drugs targeting STAT3, how close are we? Pharmacol Ther 2018; 191: 74-91.
[http://dx.doi.org/10.1016/j.pharmthera.2018.06.006] [PMID: 29933035]
[89]
Yu Y, Li S, Xu X, et al. Structural basis for the unique biological function of small GTPase RHEB. J Biol Chem 2005; 280(17): 17093-100.
[http://dx.doi.org/10.1074/jbc.M501253200] [PMID: 15728574]
[90]
Sohretoglu D, Zhang C, Luo J, Huang S. ReishiMax inhibits mTORC1/2 by activating AMPK and inhibiting IGFR/PI3K/Rheb in tumor cells. Signal Transduct Target Ther 2019; 4(1): 21.
[http://dx.doi.org/10.1038/s41392-019-0056-7] [PMID: 31637001]
[91]
Zheng H, Liu A, Liu B, Li M, Yu H, Luo X. Ras homologue enriched in brain is a critical target of farnesyltransferase inhibitors in non-small cell lung cancer cells. Cancer Lett 2010; 297(1): 117-25.
[http://dx.doi.org/10.1016/j.canlet.2010.05.004] [PMID: 20554106]
[92]
Emmanuel N, Ragunathan S, Shan Q, et al. Purine nucleotide availability regulates mTORC1 activity through the Rheb GTPase. Cell Rep 2017; 19(13): 2665-80.
[http://dx.doi.org/10.1016/j.celrep.2017.05.043] [PMID: 28658616]
[93]
Amson R, Pece S, Lespagnol A, et al. Reciprocal repression between P53 and TCTP. Nat Med 2011; 18(1): 91-9.
[http://dx.doi.org/10.1038/nm.2546] [PMID: 22157679]
[94]
Liu L-Z, Wang M, Xin Q, Wang B, Chen GG, Li M-Y. The permissive role of TCTP in PM2.5/NNK-induced epithelial-mesenchymal transition in lung cells. J Transl Med 2020; 18(1): 66.
[http://dx.doi.org/10.1186/s12967-020-02256-5] [PMID: 32046740]
[95]
Tan S, Yi P, Wang H, et al. RAC1 involves in the radioresistance by mediating epithelial-mesenchymal transition in lung cancer. Front Oncol 2020; 10: 649.
[http://dx.doi.org/10.3389/fonc.2020.00649] [PMID: 32411607]
[96]
Yang J, Qiu Q, Qian X, et al. Long noncoding RNA LCAT1 functions as a ceRNA to regulate RAC1 function by sponging miR-4715-5p in lung cancer. Mol Cancer 2019; 18(1): 171.
[http://dx.doi.org/10.1186/s12943-019-1107-y] [PMID: 31779616]
[97]
Kaneto N, Yokoyama S, Hayakawa Y, Kato S, Sakurai H, Saiki I. RAC1 inhibition as a therapeutic target for gefitinib-resistant non-small-cell lung cancer. Cancer Sci 2014; 105(7): 788-94.
[http://dx.doi.org/10.1111/cas.12425] [PMID: 24750242]
[98]
Hua K-T, Tan C-T, Johansson G, et al. N-α-acetyltransferase 10 protein suppresses cancer cell metastasis by binding PIX proteins and inhibiting CDC42/Rac1 activity. Cancer Cell 2011; 19(2): 218-31.
[http://dx.doi.org/10.1016/j.ccr.2010.11.010] [PMID: 21295525]
[99]
Stengel K, Zheng Y. CDC42 in oncogenic transformation, invasion, and tumorigenesis. Cell Signal 2011; 23(9): 1415-23.
[http://dx.doi.org/10.1016/j.cellsig.2011.04.001] [PMID: 21515363]
[100]
Aguilar BJ, Zhao Y, Zhou H, Huo S, Chen Y-H, Lu Q. Inhibition of CDC42-intersectin interaction by small molecule ZCL367 impedes cancer cell cycle progression, proliferation, migration, and tumor growth. Cancer Biol Ther 2019; 20(6): 740-9.
[http://dx.doi.org/10.1080/15384047.2018.1564559] [PMID: 30849276]

Rights & Permissions Print Cite
Article Metrics
24
1
© 2024 Bentham Science Publishers | Privacy Policy