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Volume 25, Issue 4
  • ISSN: 1568-0096
  • E-ISSN: 1873-5576
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Abstract

Background

Lung adenocarcinoma (LUAD) is a highly lethal malignancy. Liquid-Liquid Phase Separation (LLPS) plays a crucial role in targeted therapies for lung cancer and in the progression of lung squamous cell carcinoma. However, the role of LLPS in the progression and prognosis of LUAD remains insufficiently explored.

Methods

This study employed a multi-step approach to identify LLPS prognosis-related genes in LUAD. First, differential analysis, univariate Cox regression analysis, Random Survival Forest (RSF) method, and Least Absolute Shrinkage and Selection Operator (LASSO) Cox regression analysis were utilized to identify five LLPS prognosis-related genes. Subsequently, LASSO Cox regression was performed to establish a prognostic score termed the LLPS-related prognosis score (LPRS). Comprehensive analyses were then conducted based on the LPRS, including survival analysis, clinical feature analysis, functional enrichment analysis, and tumor microenvironment assessment. The LPRS was integrated with additional clinicopathological factors to develop a prognostic nomogram for LUAD patients. Immunohistochemical validation was performed on clinical tissue samples to further validate the findings. Finally, the relationship between KRT6A, one of the identified genes, and epidermal growth factor receptor (EGFR) mutations was investigated.

Results

The LPRS was established using five LLPS-related genes: IGF2BP1, KRT6A, LDHA, PKP2, and PLK1. Higher LPRS was closely associated with poor survival outcomes, gender, progression-free survival (PFS), and advanced TNM stage. Furthermore, LPRS emerged as an independent prognostic factor for LUAD. A nomogram integrating LPRS, TNM stage, and age demonstrated remarkable predictive accuracy for prognosis among patients with LUAD. LLPS likely influences LUAD prognosis through the activity of IGF2BP1, KRT6A, LDHA, PKP2, and PLK1. KRT6A exhibits significant upregulation in LUAD, particularly in patients with EGFR mutations.

Conclusion

This study introduces a novel LPRS model that demonstrates high accuracy in predicting the clinical prognosis of LUAD. Moreover, the findings suggest that KRT6A may play a critical role in the LLPS-mediated malignant progression of LUAD.

© 2025 Bentham Science Publishers
© 2025 The Author(s). Published by Bentham Science Publishers. This is an open access article published under CC BY 4.0 https://creativecommons.org/licenses/by/4.0/legalcode
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2025-04-16

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References

  1. ThaiA.A. SolomonB.J. SequistL.V. GainorJ.F. HeistR.S. Lung cancer.Lancet20213981029953555410.1016/S0140‑6736(21)00312‑334273294
     [Google Scholar]
  2. FordeP.M. SpicerJ. LuS. ProvencioM. MitsudomiT. AwadM.M. FelipE. BroderickS.R. BrahmerJ.R. SwansonS.J. KerrK. WangC. CiuleanuT.E. SaylorsG.B. TanakaF. ItoH. ChenK.N. LibermanM. VokesE.E. TaubeJ.M. DorangeC. CaiJ. FioreJ. JarkowskiA. BalliD. SausenM. PandyaD. CalvetC.Y. GirardN. Neoadjuvant nivolumab plus chemotherapy in resectable lung cancer.N. Engl. J. Med.2022386211973198510.1056/NEJMoa220217035403841
     [Google Scholar]
  3. LiY. YanB. HeS. Advances and challenges in the treatment of lung cancer.Biomed. Pharmacother.202316911589110.1016/j.biopha.2023.11589137979378
     [Google Scholar]
  4. AbdelazizH.M. GaberM. Abd-ElwakilM.M. MabroukM.T. ElgoharyM.M. KamelN.M. KabaryD.M. FreagM.S. SamahaM.W. MortadaS.M. ElkhodairyK.A. FangJ.Y. ElzoghbyA.O. Inhalable particulate drug delivery systems for lung cancer therapy: Nanoparticles, microparticles, nanocomposites and nanoaggregates.J. Control. Release201826937439210.1016/j.jconrel.2017.11.03629180168
     [Google Scholar]
  5. SchabathM.B. CoteM.L. Cancer progress and priorities: Lung cancer.Cancer Epidemiol. Biomarkers Prev.201928101563157910.1158/1055‑9965.EPI‑19‑022131575553
     [Google Scholar]
  6. ShiF. LiL. Phosphatidylinositol 3-Kinase/Protein Kinase B/Mammalian Target of the Rapamycin Pathway-Related Protein Expression in Lung Squamous Cell Carcinoma and Its Correlation with Lymph Node Metastasis.J. Oncol.202220221710.1155/2022/453725636052284
     [Google Scholar]
  7. WuJ. LinZ. Non-small cell lung cancer targeted therapy: Drugs and mechanisms of drug resistance.Int. J. Mol. Sci.202223231505610.3390/ijms23231505636499382
     [Google Scholar]
  8. ImyanitovE.N. IyevlevaA.G. LevchenkoE.V. Molecular testing and targeted therapy for non-small cell lung cancer: Current status and perspectives.Crit. Rev. Oncol. Hematol.202115710319410.1016/j.critrevonc.2020.10319433316418
     [Google Scholar]
  9. TanA.C. TanD.S.W. Targeted therapies for lung cancer patients with oncogenic driver molecular alterations.J. Clin. Oncol.202240661162510.1200/JCO.21.0162634985916
     [Google Scholar]
  10. Herrera-JuárezM. Serrano-GómezC. Bote-de-CaboH. Paz-AresL. Targeted therapy for lung cancer: Beyond EGFR and ALK.Cancer2023129121803182010.1002/cncr.3475737073562
     [Google Scholar]
  11. HirschF.R. ScagliottiG.V. MulshineJ.L. KwonR. CurranW.J.Jr WuY.L. Paz-AresL. Lung cancer: current therapies and new targeted treatments.Lancet20173891006629931110.1016/S0140‑6736(16)30958‑827574741
     [Google Scholar]
  12. FuK. XieF. WangF. FuL. Therapeutic strategies for EGFR-mutated non-small cell lung cancer patients with osimertinib resistance.J. Hematol. Oncol.202215117310.1186/s13045‑022‑01391‑436482474
     [Google Scholar]
  13. ChenP. LiuY. WenY. ZhouC. Non‐small cell lung cancer in China.Cancer Commun. (Lond.)2022421093797010.1002/cac2.1235936075878
     [Google Scholar]
  14. ZomboriT. SejbenA. TiszlaviczL. CserniG. PálföldiR. CsadaE. FurákJ. Architectural Grade Combined With Spread Through Air Spaces (STAS) Predicts Recurrence and is Suitable for Stratifying Patients Who Might Be Eligible for Lung Sparing Surgery for Stage I Adenocarcinomas.Pathol. Oncol. Res.20202642451245810.1007/s12253‑020‑00855‑732564261
     [Google Scholar]
  15. HeJ. HuangZ. HanL. GongY. XieC. Mechanisms and management of 3rd‑generation EGFR‑TKI resistance in advanced non‑small cell lung cancer.Int. J. Oncol.20215959010.3892/ijo.2021.527034558640
     [Google Scholar]
  16. BlaquierJ.B. Ortiz-CuaranS. RicciutiB. MezquitaL. CardonaA.F. RecondoG. Tackling osimertinib resistance in EGFR-mutant non–small cell lung cancer.Clin. Cancer Res.202329183579359110.1158/1078‑0432.CCR‑22‑191237093192
     [Google Scholar]
  17. PassaroA. JänneP.A. MokT. PetersS. Overcoming therapy resistance in EGFR-mutant lung cancer.Nat. Cancer20212437739110.1038/s43018‑021‑00195‑835122001
     [Google Scholar]
  18. BertoliE. De CarloE. Del ConteA. StanzioneB. RevelantA. FassettaK. SpinaM. BearzA. Acquired resistance to osimertinib in EGFR-mutated non-small cell lung cancer: How do we overcome it?Int. J. Mol. Sci.20222313693610.3390/ijms2313693635805940
     [Google Scholar]
  19. CooperA.J. SequistL.V. LinJ.J. Third-generation EGFR and ALK inhibitors: Mechanisms of resistance and management.Nat. Rev. Clin. Oncol.202219849951410.1038/s41571‑022‑00639‑935534623
     [Google Scholar]
  20. MehtaS. ZhangJ. Liquid–liquid phase separation drives cellular function and dysfunction in cancer.Nat. Rev. Cancer202222423925210.1038/s41568‑022‑00444‑735149762
     [Google Scholar]
  21. Szała-MendykB. PhanT.M. MohantyP. MittalJ. Challenges in studying the liquid-to-solid phase transitions of proteins using computer simulations.Curr. Opin. Chem. Biol.20237510233310.1016/j.cbpa.2023.10233337267850
     [Google Scholar]
  22. BrachaD. WallsM.T. BrangwynneC.P. Probing and engineering liquid-phase organelles.Nat. Biotechnol.201937121435144510.1038/s41587‑019‑0341‑631792412
     [Google Scholar]
  23. AlbertiS. HymanA.A. Biomolecular condensates at the nexus of cellular stress, protein aggregation disease and ageing.Nat. Rev. Mol. Cell Biol.202122319621310.1038/s41580‑020‑00326‑633510441
     [Google Scholar]
  24. WiednerH.J. GiudiceJ. It’s not just a phase: Function and characteristics of RNA-binding proteins in phase separation.Nat. Struct. Mol. Biol.202128646547310.1038/s41594‑021‑00601‑w34099940
     [Google Scholar]
  25. WaghK. GarciaD.A. UpadhyayaA. Phase separation in transcription factor dynamics and chromatin organization.Curr. Opin. Struct. Biol.20217114815510.1016/j.sbi.2021.06.00934303933
     [Google Scholar]
  26. ChengY. XieW. PickeringB.F. ChuK.L. SavinoA.M. YangX. LuoH. NguyenD.T.T. MoS. BarinE. VellecaA. RohwetterT.M. PatelD.J. JaffreyS.R. KharasM.G. N6-Methyladenosine on mRNA facilitates a phase-separated nuclear body that suppresses myeloid leukemic differentiation.Cancer Cell2021397958972.e810.1016/j.ccell.2021.04.01734048709
     [Google Scholar]
  27. PakravanD. OrlandoG. BercierV. Van Den BoschL. Role and therapeutic potential of liquid–liquid phase separation in amyotrophic lateral sclerosis.J. Mol. Cell Biol.2021131152810.1093/jmcb/mjaa04932976566
     [Google Scholar]
  28. KanekuraK. KurodaM. How can we interpret the relationship between liquid-liquid phase separation and amyotrophic lateral sclerosis?Lab. Invest.2022102991291810.1038/s41374‑022‑00791‑x35459796
     [Google Scholar]
  29. AinaniH. BouchmaaN. Ben MridR. El FatimyR. Liquid-liquid phase separation of protein tau: An emerging process in Alzheimer’s disease pathogenesis.Neurobiol. Dis.202317810601110.1016/j.nbd.2023.10601136702317
     [Google Scholar]
  30. BoykoS. SurewiczW.K. Tau liquid–liquid phase separation in neurodegenerative diseases.Trends Cell Biol.202232761162310.1016/j.tcb.2022.01.01135181198
     [Google Scholar]
  31. FuQ. ZhangB. ChenX. ChuL. Liquid–liquid phase separation in Alzheimer’s disease.J. Mol. Med. (Berl.)2024102216718110.1007/s00109‑023‑02407‑338167731
     [Google Scholar]
  32. RelliV. TrerotolaM. GuerraE. AlbertiS. Abandoning the notion of non-small cell lung cancer.Trends Mol. Med.201925758559410.1016/j.molmed.2019.04.01231155338
     [Google Scholar]
  33. WangB. ZhangL. DaiT. QinZ. LuH. ZhangL. ZhouF. Liquid–liquid phase separation in human health and diseases.Signal Transduct. Target. Ther.20216129010.1038/s41392‑021‑00678‑134334791
     [Google Scholar]
  34. ZouY. ZhengH. NingY. YangY. WenQ. FanS. New insights into the important roles of phase seperation in the targeted therapy of lung cancer.Cell Biosci.202313115010.1186/s13578‑023‑01101‑837580790
     [Google Scholar]
  35. KleinI.A. BoijaA. AfeyanL.K. HawkenS.W. FanM. Dall’AgneseA. OksuzO. HenningerJ.E. ShrinivasK. SabariB.R. SagiI. ClarkV.E. PlattJ.M. KarM. McCallP.M. ZamudioA.V. ManteigaJ.C. CoffeyE.L. LiC.H. HannettN.M. GuoY.E. DeckerT.M. LeeT.I. ZhangT. WengJ.K. TaatjesD.J. ChakrabortyA. SharpP.A. ChangY.T. HymanA.A. GrayN.S. YoungR.A. Partitioning of cancer therapeutics in nuclear condensates.Science202036864971386139210.1126/science.aaz442732554597
     [Google Scholar]
  36. TongX. TangR. XuJ. WangW. ZhaoY. YuX. ShiS. Liquid–liquid phase separation in tumor biology.Signal Transduct. Target. Ther.20227122110.1038/s41392‑022‑01076‑x35803926
     [Google Scholar]
  37. PengP-H. HsuK-W. WuK-J. Liquid-liquid phase separation (LLPS) in cellular physiology and tumor biology.Am. J. Cancer Res.20211183766377634522448
     [Google Scholar]
  38. LiuZ. QinZ. LiuY. XiaX. HeL. ChenN. HuX. PengX. Liquid‒liquid phase separation: roles and implications in future cancer treatment.Int. J. Biol. Sci.202319134139415610.7150/ijbs.8152137705755
     [Google Scholar]
  39. XieQ. ChengJ. MeiW. YangD. ZhangP. ZengC. Phase separation in cancer at a glance.J. Transl. Med.202321123710.1186/s12967‑023‑04082‑x37005672
     [Google Scholar]
  40. XiaoC. WuG. ChenP. GaoL. ChenG. ZhangH. Phase separation in epigenetics and cancer stem cells.Front. Oncol.20221292260410.3389/fonc.2022.92260436081552
     [Google Scholar]
  41. PengQ. TanS. XiaL. WuN. OyangL. TangY. SuM. LuoX. WangY. ShengX. ZhouY. LiaoQ. Phase separation in Cancer: From the Impacts and Mechanisms to Treatment potentials.Int. J. Biol. Sci.202218135103512210.7150/ijbs.7541035982902
     [Google Scholar]
  42. JiangX. ZhangY. WangH. WangZ. HuS. CaoC. XiaoH. In-depth metaproteomics analysis of oral microbiome for lung cancer.Research202220222022/978157810.34133/2022/978157836320634
     [Google Scholar]
  43. LiuC. QinQ. CongH. Research progress on the relationship between mitochondrial deoxyguanosine kinase and apoptosis and autophagy in lung adenocarcinoma cells.Cancer Insight202211810.58567/ci01010004
     [Google Scholar]
  44. HuangH. WengH. SunW. QinX. ShiH. WuH. ZhaoB.S. MesquitaA. LiuC. YuanC.L. HuY.C. HüttelmaierS. SkibbeJ.R. SuR. DengX. DongL. SunM. LiC. NachtergaeleS. WangY. HuC. FerchenK. GreisK.D. JiangX. WeiM. QuL. GuanJ.L. HeC. YangJ. ChenJ. Recognition of RNA N6-methyladenosine by IGF2BP proteins enhances mRNA stability and translation.Nat. Cell Biol.201820328529510.1038/s41556‑018‑0045‑z29476152
     [Google Scholar]
  45. KornS.M. UlshöferC.J. SchneiderT. SchlundtA. Structures and target RNA preferences of the RNA-binding protein family of IGF2BPs: An overview.Structure202129878780310.1016/j.str.2021.05.00134022128
     [Google Scholar]
  46. PengW. YeL. XueQ. WeiX. WangZ. XiangX. ZhangS. ZhangP. WangH. ZhouQ. Silencing of circCRIM1 Drives IGF2BP1-Mediated NSCLC Immune Evasion.Cells202312227310.3390/cells1202027336672208
     [Google Scholar]
  47. ZhuQ. ZhangC. QuT. LuX. HeX. LiW. YinD. HanL. GuoR. ZhangE. MNX1-AS1 promotes phase separation of IGF2BP1 to Drive c-Myc–mediated cell-cycle progression and proliferation in lung cancer.Cancer Res.202282234340435810.1158/0008‑5472.CAN‑22‑128936214649
     [Google Scholar]
  48. ZengW. LuC. ShiY. WuC. ChenX. LiC. YaoJ. Initiation of stress granule assembly by rapid clustering of IGF2BP proteins upon osmotic shock.Biochim. Biophys. Acta Mol. Cell Res.202018671011879510.1016/j.bbamcr.2020.11879532668274
     [Google Scholar]
  49. YangB. ZhangW. ZhangM. WangX. PengS. ZhangR. KRT6A promotes EMT and cancer stem cell transformation in lung adenocarcinoma.Technol. Cancer Res. Treat.20201910.1177/153303382092124832329414
     [Google Scholar]
  50. XiaoJ. LuX. ChenX. ZouY. LiuA. LiW. HeB. HeS. ChenQ. Eight potential biomarkers for distinguishing between lung adenocarcinoma and squamous cell carcinoma.Oncotarget2017842717597177110.18632/oncotarget.1760629069744
     [Google Scholar]
  51. ZhouJ. JiangG. XuE. ZhouJ. LiuL. YangQ. Identification of SRXN1 and KRT6A as key genes in smoking-related non-small-cell lung cancer through bioinformatics and functional analyses.Front. Oncol.20221181030110.3389/fonc.2021.81030135071014
     [Google Scholar]
  52. CheD. WangM. SunJ. LiB. XuT. LuY. PanH. LuZ. GuX. KRT6A promotes lung cancer cell growth and invasion through MYC-regulated pentose phosphate pathway.Front. Cell Dev. Biol.2021969407110.3389/fcell.2021.69407134235156
     [Google Scholar]
  53. BaiY. QiW. LiuL. ZhangJ. PangL. GanT. WangP. WangC. ChenH. Identification of seven-gene hypoxia signature for predicting overall survival of hepatocellular carcinoma.Front. Genet.20211263741810.3389/fgene.2021.63741833912215
     [Google Scholar]
  54. YuX. ZhangX. ZhangY. Identification of a 5-gene metabolic signature for predicting prognosis based on an integrated analysis of tumor microenvironment in lung adenocarcinoma.J. Oncol.2020202011210.1155/2020/531079332684932
     [Google Scholar]
  55. ComandatoreA. FranczakM. SmolenskiR.T. MorelliL. PetersG.J. GiovannettiE. Lactate Dehydrogenase and its clinical significance in pancreatic and thoracic cancers.Semin. Cancer Biol.202286Pt 29310010.1016/j.semcancer.2022.09.00136096316
     [Google Scholar]
  56. HaoX.L. TianZ. HanF. ChenJ.P. GaoL.Y. LiuJ.Y. Plakophilin-2 accelerates cell proliferation and migration through activating EGFR signaling in lung adenocarcinoma.Pathol. Res. Pract.2019215715243810.1016/j.prp.2019.15243831126818
     [Google Scholar]
  57. CongD. ZhaoY. ZhangW. LiJ. BaiY. Applying machine learning algorithms to develop a survival prediction model for lung adenocarcinoma based on genes related to fatty acid metabolism.Front. Pharmacol.202314126074210.3389/fphar.2023.126074237920207
     [Google Scholar]
  58. WuY. LiuL. ShenX. LiuW. MaR. Plakophilin-2 promotes lung adenocarcinoma development via enhancing focal adhesion and epithelial–mesenchymal transition.Cancer Manag. Res.20211355957010.2147/CMAR.S28166333519235
     [Google Scholar]
  59. ArimotoK. BurkartC. YanM. RanD. WengS. ZhangD.E. Plakophilin-2 promotes tumor development by enhancing ligand-dependent and -independent epidermal growth factor receptor dimerization and activation.Mol. Cell. Biol.201434203843385410.1128/MCB.00758‑1425113560
     [Google Scholar]
  60. LiuZ. SunQ. WangX. PLK1, a potential target for cancer therapy.Transl. Oncol.2017101223210.1016/j.tranon.2016.10.00327888710
     [Google Scholar]
  61. IliakiS. BeyaertR. AfoninaI.S. Polo-like kinase 1 (PLK1) signaling in cancer and beyond.Biochem. Pharmacol.202119311474710.1016/j.bcp.2021.11474734454931
     [Google Scholar]
  62. SuS. ChhabraG. SinghC.K. NdiayeM.A. AhmadN. PLK1 inhibition-based combination therapies for cancer management.Transl. Oncol.20221610133210.1016/j.tranon.2021.10133234973570
     [Google Scholar]
  63. WangZ.X. XueD. LiuZ.L. LuB.B. BianH.B. PanX. YinY.M. Overexpression of polo-like kinase 1 and its clinical significance in human non-small cell lung cancer.Int. J. Biochem. Cell Biol.201244120021010.1016/j.biocel.2011.10.01722064247
     [Google Scholar]
  64. RedaM. NgamcherdtrakulW. GuS. BejanD.S. SiriwonN. GrayJ.W. YantaseeW. PLK1 and EGFR targeted nanoparticle as a radiation sensitizer for non-small cell lung cancer.Cancer Lett.201946791810.1016/j.canlet.2019.09.01431563561
     [Google Scholar]
  65. InoueM. YoshimuraM. KobayashiM. MorinibuA. ItasakaS. HiraokaM. HaradaH. PLK1 blockade enhances therapeutic effects of radiation by inducing cell cycle arrest at the mitotic phase.Sci. Rep.2015511566610.1038/srep1566626503893
     [Google Scholar]
  66. BoijaA. KleinI.A. YoungR.A. Biomolecular Condensates and Cancer.Cancer Cell202139217419210.1016/j.ccell.2020.12.00333417833
     [Google Scholar]
  67. ZhanY. WangH. NingY. ZhengH. LiuS. YangY. ZhouM. FanS. Understanding the roles of stress granule during chemotherapy for patients with malignant tumors.Am. J. Cancer Res.20201082226224132905441
     [Google Scholar]
  68. ZhangJ. ZengY. XingY. LiX. ZhouL. HuL. ChinY.E. WuM. Myristoylation-mediated phase separation of EZH2 compartmentalizes STAT3 to promote lung cancer growth.Cancer Lett.2021516849810.1016/j.canlet.2021.05.03534102285
     [Google Scholar]
  69. GrabarzA. BarascuA. Guirouilh-BarbatJ. LopezB.S. Initiation of DNA double strand break repair: signaling and single-stranded resection dictate the choice between homologous recombination, non-homologous end-joining and alternative end-joining.Am. J. Cancer Res.20122324926822679557
     [Google Scholar]
  70. WuY. ZhouL. ZouY. ZhangY. ZhangM. XuL. ZhengL. HeW. YuK. LiT. ZhangX. ChenZ. ZhangR. ZhouP. ZhangN. ZhengL. KangT. Disrupting the phase separation of KAT8–IRF1 diminishes PD-L1 expression and promotes antitumor immunity.Nat. Cancer20234338240010.1038/s43018‑023‑00522‑136894639
     [Google Scholar]
  71. QinZ. SunH. YueM. PanX. ChenL. FengX. YanX. ZhuX. JiH. Phase separation of EML4–ALK in firing downstream signaling and promoting lung tumorigenesis.Cell Discov.2021713310.1038/s41421‑021‑00270‑533976114
     [Google Scholar]
  72. LinS.Y. MakinoK. XiaW. MatinA. WenY. KwongK.Y. BourguignonL. HungM.C. Nuclear localization of EGF receptor and its potential new role as a transcription factor.Nat. Cell Biol.20013980280810.1038/ncb0901‑80211533659
     [Google Scholar]
  73. HanadaN. LoH.W. DayC.P. PanY. NakajimaY. HungM.C. Co‐regulation of B‐Myb expression by E2F1 and EGF receptor.Mol. Carcinog.2006451101710.1002/mc.2014716299810
     [Google Scholar]
  74. ShenM. ZhangR. JiaW. ZhuZ. ZhaoL. HuangG. LiuJ. RNA-binding protein p54nrb/NONO potentiates nuclear EGFR-mediated tumorigenesis of triple-negative breast cancer.Cell Death Dis.20221314210.1038/s41419‑021‑04488‑935013116
     [Google Scholar]
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Liquid-Liquid Phase Separation in the Prognosis of Lung Adenocarcinoma: An Integrated Analysis
Curr. Cancer Drug Targets< 25, 323 (2025); https://doi.org/10.2174/0115680096345676241001081051
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  • Article Type:     Research Article
Keyword(s): EGFR; IGF2BP1; KRT6A; liquid-liquid phase separation; Lung adenocarcinoma; prognosis

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