دورية أكاديمية
Long non-coding RNA MAGEA4-AS1 binding to p53 enhances MK2 signaling pathway and promotes the proliferation and metastasis of oral squamous cell carcinoma.
| العنوان: | Long non-coding RNA MAGEA4-AS1 binding to p53 enhances MK2 signaling pathway and promotes the proliferation and metastasis of oral squamous cell carcinoma. |
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| المؤلفون: | Wei X; Peking University Shenzhen Hospital Clinical College, The Fifth School of Clinical Medicine, Anhui Medical University, Hefei, Anhui, 230032, China.; Department of Oral and Maxillofacial Surgery, Stomatological Center, Peking University Shenzhen Hospital, Guangdong Provincial High-level Clinical Key Specialty, Guangdong Province Engineering Research Center of Oral Disease Diagnosis and Treatment, The Institute of Stomatology, Shenzhen Peking University-The Hong Kong University of Science and Technology Medical Center, Shenzhen, Guangdong, 518036, China., Li Z; Department of Oral and Maxillofacial Surgery, Stomatological Center, Peking University Shenzhen Hospital, Guangdong Provincial High-level Clinical Key Specialty, Guangdong Province Engineering Research Center of Oral Disease Diagnosis and Treatment, The Institute of Stomatology, Shenzhen Peking University-The Hong Kong University of Science and Technology Medical Center, Shenzhen, Guangdong, 518036, China., Zheng H; Peking University Shenzhen Hospital Clinical College, The Fifth School of Clinical Medicine, Anhui Medical University, Hefei, Anhui, 230032, China.; Department of Oral and Maxillofacial Surgery, Stomatological Center, Peking University Shenzhen Hospital, Guangdong Provincial High-level Clinical Key Specialty, Guangdong Province Engineering Research Center of Oral Disease Diagnosis and Treatment, The Institute of Stomatology, Shenzhen Peking University-The Hong Kong University of Science and Technology Medical Center, Shenzhen, Guangdong, 518036, China., Li X; Department of Oral and Maxillofacial Surgery, Stomatological Center, Peking University Shenzhen Hospital, Guangdong Provincial High-level Clinical Key Specialty, Guangdong Province Engineering Research Center of Oral Disease Diagnosis and Treatment, The Institute of Stomatology, Shenzhen Peking University-The Hong Kong University of Science and Technology Medical Center, Shenzhen, Guangdong, 518036, China., Lin Y; Department of Oral and Maxillofacial Surgery, Stomatological Center, Peking University Shenzhen Hospital, Guangdong Provincial High-level Clinical Key Specialty, Guangdong Province Engineering Research Center of Oral Disease Diagnosis and Treatment, The Institute of Stomatology, Shenzhen Peking University-The Hong Kong University of Science and Technology Medical Center, Shenzhen, Guangdong, 518036, China., Yang H; Peking University Shenzhen Hospital Clinical College, The Fifth School of Clinical Medicine, Anhui Medical University, Hefei, Anhui, 230032, China. yanghongyu@ahmu.edu.cn.; Department of Oral and Maxillofacial Surgery, Stomatological Center, Peking University Shenzhen Hospital, Guangdong Provincial High-level Clinical Key Specialty, Guangdong Province Engineering Research Center of Oral Disease Diagnosis and Treatment, The Institute of Stomatology, Shenzhen Peking University-The Hong Kong University of Science and Technology Medical Center, Shenzhen, Guangdong, 518036, China. yanghongyu@ahmu.edu.cn., Shen Y; Peking University Shenzhen Hospital Clinical College, The Fifth School of Clinical Medicine, Anhui Medical University, Hefei, Anhui, 230032, China. yhshen@pkuszh.com.; Department of Oral and Maxillofacial Surgery, Stomatological Center, Peking University Shenzhen Hospital, Guangdong Provincial High-level Clinical Key Specialty, Guangdong Province Engineering Research Center of Oral Disease Diagnosis and Treatment, The Institute of Stomatology, Shenzhen Peking University-The Hong Kong University of Science and Technology Medical Center, Shenzhen, Guangdong, 518036, China. yhshen@pkuszh.com. |
| المصدر: | Functional & integrative genomics [Funct Integr Genomics] 2024 Sep 09; Vol. 24 (5), pp. 158. Date of Electronic Publication: 2024 Sep 09. |
| نوع المنشور: | Journal Article |
| اللغة: | English |
| بيانات الدورية: | Publisher: Springer Country of Publication: Germany NLM ID: 100939343 Publication Model: Electronic Cited Medium: Internet ISSN: 1438-7948 (Electronic) Linking ISSN: 1438793X NLM ISO Abbreviation: Funct Integr Genomics Subsets: MEDLINE |
| أسماء مطبوعة: | Original Publication: Berlin : Springer, c2000- |
| مواضيع طبية MeSH: | RNA, Long Noncoding*/genetics , RNA, Long Noncoding*/metabolism , Cell Proliferation* , Tumor Suppressor Protein p53*/metabolism , Tumor Suppressor Protein p53*/genetics , Mouth Neoplasms*/genetics , Mouth Neoplasms*/metabolism , Mouth Neoplasms*/pathology , Signal Transduction* , Intracellular Signaling Peptides and Proteins*/metabolism , Intracellular Signaling Peptides and Proteins*/genetics , Cell Movement* , Protein Serine-Threonine Kinases*/metabolism , Protein Serine-Threonine Kinases*/genetics, Humans ; Cell Line, Tumor ; Carcinoma, Squamous Cell/genetics ; Carcinoma, Squamous Cell/metabolism ; Carcinoma, Squamous Cell/pathology ; Gene Expression Regulation, Neoplastic ; Female ; Male ; Neoplasm Metastasis |
| مستخلص: | Long non-coding RNAs (lncRNAs) regulate the occurrence, development and progression of oral squamous cell carcinoma (OSCC). We elucidated the expression features of MAGEA4-AS1 in patients with OSCC and its activity as an OSCC biomarker. Furthermore, the impact of up-regulation of MAGEA4-AS1 on the cellular behaviors (proliferation, migration and invasion) of OSCC cells and intrinsic signal mechanisms were evaluated. Firstly, we analyzed MAGEA4-AS1 expression data in The Cancer Genome Atlas (TCGA) OSCC using a bioinformatics approach and in 45 pairs of OSCC tissues using qPCR. Then CCK-8, ethynyl deoxyuridine, colony formation, transwell and wound healing assays were conducted to assess changes in the cell proliferation, migration and invasion protential of shMAGEA4-AS1 HSC3 and CAL27 cells. The RNA sequence of MAGEA4-AS1 was identified using the rapid amplification of cDNA ends (RACE) assay. And whole-transcriptome sequencing was used to identify MAGEA4-AS1 affected genes. Additionally, dual-luciferase reporter system, RNA-binding protein immunoprecipitation (RIP), and rescue experiments were performed to clarify the role of the MAGEA4-AS1-p53-MK2 signaling pathway. As results, we found MAGEA4-AS1 was up-regulated in OSCC tissues. We identified a 418 nucleotides length of the MAGEA4-AS1 transcript and it primarily located in the cell nucleus. MAGEA4-AS1 stable knockdown weakened the proliferation, migration and invasion abilities of OSCC cells. Mechanistically, p53 protein was capable to activate MK2 gene transcription. RIP assay revealed an interaction between p53 and MAGEA4-AS1. MK2 up-regulation in MAGEA4-AS1 down-regulated OSCC cells restored MK2 and epithelial-to-mesenchymal transition related proteins' expression levels. In conclusion, MAGEA4-AS1-p53 complexes bind to MK2 promoter, enhancing the transcription of MK2 and activating the downstream signaling pathways, consequently promoting the proliferation and metastasis of OSCC cells. MAGEA4-AS1 may serve as a diagnostic marker and therapeutic target for OSCC patients. (© 2024. The Author(s).) |
| References: | Nat Rev Mol Cell Biol. 2022 Dec;23(12):853. (PMID: 36229539) Trends Cell Biol. 2011 Jun;21(6):354-61. (PMID: 21550244) Oral Oncol. 2021 Oct;121:105451. (PMID: 34329869) Theranostics. 2022 Oct 17;12(17):7351-7370. (PMID: 36438499) Mol Cancer. 2020 Jul 29;19(1):118. (PMID: 32727463) J Exp Clin Cancer Res. 2019 Aug 20;38(1):365. (PMID: 31429766) Cell Cycle. 2022 Sep;21(17):1856-1866. (PMID: 35604743) Cell Cycle. 2020 Jul;19(13):1641-1653. (PMID: 32450050) Front Oncol. 2021 Feb 25;10:624752. (PMID: 33732637) Cancer Res. 2017 Aug 1;77(15):3965-3981. (PMID: 28701486) Cancer Res. 2010 Jan 15;70(2):832-41. (PMID: 20068172) Oral Oncol. 2015 Aug;51(8):738-44. (PMID: 25987307) JAMA Oncol. 2020 Oct 1;6(10):1563-1570. (PMID: 32852531) CA Cancer J Clin. 2023 Jan;73(1):17-48. (PMID: 36633525) Cancer Cell. 2016 Apr 11;29(4):452-463. (PMID: 27070700) Proc Natl Acad Sci U S A. 2018 Jun 12;115(24):E5546-E5555. (PMID: 29844172) Carcinogenesis. 2009 Dec;30(12):2100-8. (PMID: 19808857) Mol Cell. 2011 Sep 16;43(6):904-14. (PMID: 21925379) Nat Rev Mol Cell Biol. 2023 Jun;24(6):430-447. (PMID: 36596869) Nature. 2021 Jan;589(7842):448-455. (PMID: 33328637) Radiother Oncol. 2019 May;134:1-9. (PMID: 31005201) Trends Cell Biol. 2019 Mar;29(3):212-226. (PMID: 30594349) Genet Epidemiol. 2014 May;38(4):275-80. (PMID: 24723339) Trends Genet. 2021 Aug;37(8):695-698. (PMID: 33892960) Clin Transl Med. 2022 Apr;12(4):e792. (PMID: 35415876) Nat Rev Clin Oncol. 2019 Nov;16(11):669-683. (PMID: 31189965) Mol Cancer. 2022 Apr 27;21(1):105. (PMID: 35477447) J Zhejiang Univ Sci B. 2023 Sept 15;24(9):796-806. (PMID: 37701956) Biosci Rep. 2020 Apr 30;40(4):. (PMID: 32202300) J Exp Clin Cancer Res. 2019 Mar 8;38(1):121. (PMID: 30850014) EMBO J. 2024 Apr;43(7):1273-1300. (PMID: 38448672) J Cell Mol Med. 2020 Dec;24(24):14392-14404. (PMID: 33145952) Front Mol Biosci. 2022 Aug 29;9:942636. (PMID: 36106022) Mol Cell. 2022 Jun 16;82(12):2252-2266. (PMID: 35714586) Cell Death Dis. 2022 Nov 7;13(11):936. (PMID: 36344495) Mol Ther. 2018 Apr 4;26(4):1066-1081. (PMID: 29525743) Cancer Commun (Lond). 2022 Feb;42(2):117-140. (PMID: 35019235) Nature. 1994 Dec 22-29;372(6508):739-46. (PMID: 7997261) Trends Biochem Sci. 2016 Sep;41(9):761-772. (PMID: 27499234) Cell. 2013 Mar 14;152(6):1298-307. (PMID: 23498938) J Exp Clin Cancer Res. 2020 Dec 2;39(1):270. (PMID: 33267897) Nat Rev Mol Cell Biol. 2022 Jun;23(6):389-406. (PMID: 35079163) |
| معلومات مُعتمدة: | JCYJ20220531094216037 Shenzhen Science and Technology Program; JCYJ20200109140208058 Shenzhen Science and Technology Program; 20210617170745001 Shenzhen Clinical Research Center for Oral Diseases; SZSM 202111012 the Sanming Project of Medicine in Shenzhen; No. SZGSP008 Shenzhen Fund for Guangdong Provincial High-level Clinical Key Specialties; KYQD2023253 Shenzhen High-level Hospital Construction Fund, Peking University Shenzhen Hospital Scientific Research Fund |
| فهرسة مساهمة: | Keywords: EMT; MAGEA4-AS1; MK2; Transcription regulation; lncRNAs; p53 |
| المشرفين على المادة: | 0 (RNA, Long Noncoding) 0 (Tumor Suppressor Protein p53) 0 (Intracellular Signaling Peptides and Proteins) EC 2.7.1.- (MAP-kinase-activated kinase 2) EC 2.7.11.1 (Protein Serine-Threonine Kinases) 0 (TP53 protein, human) |
| تواريخ الأحداث: | Date Created: 20240909 Date Completed: 20240909 Latest Revision: 20240912 |
| رمز التحديث: | 20240912 |
| مُعرف محوري في PubMed: | PMC11384635 |
| DOI: | 10.1007/s10142-024-01436-6 |
| PMID: | 39249547 |
| قاعدة البيانات: | MEDLINE |
Find this article in full text from Springer Verlag. 
Full Text Finder | تدمد: | 1438-7948 |
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| DOI: | 10.1007/s10142-024-01436-6 |