TRIM6 Promotes Cell Cycle and Growth by Modulating p53 Signaling Pathway in Lung Adenocarcinoma

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Pubblicato in:International Journal of General Medicine vol. 18 (2025), p. 2107
Autore principale: Lu, Xi
Altri autori: Wang, Haifeng, Yu, Tingting
Pubblicazione:
Taylor & Francis Ltd.
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LEADER 00000nab a2200000uu 4500
001 3190895342
003 UK-CbPIL
022 |a 1178-7074 
024 7 |a 10.2147/IJGM.S497383  |2 doi 
035 |a 3190895342 
045 2 |b d20250101  |b d20251231 
100 1 |a Lu, Xi 
245 1 |a TRIM6 Promotes Cell Cycle and Growth by Modulating p53 Signaling Pathway in Lung Adenocarcinoma 
260 |b Taylor & Francis Ltd.  |c 2025 
513 |a Journal Article 
520 3 |a Objective: Accumulated evidence suggested that tripartite motif-containing (TRIM) proteins have a pivotal role in cancer progression. The function of TRIM6 remains largely unknown in lung adenocarcinoma (LUAD). This study aimed to clarify the role of TRIM6 in the LUAD pathogenesis.Methods: The genes involved in TRIM were selected by differential gene expression analysis and Cox regression analysis. TRIM6 was identified and verified in LUAD specimens and in paired normal tissues using immunohistochemistry. A correlation analysis was conducted comparing the expression of TRIM6 and clinicopathologic features. The role of TRIM6 in vitro and in vivo was evaluated by cell proliferation assays, cell apoptosis, cell cycle and a tumor xenograft model. Finally, we investigated downstream proteins regulated by TRIM6 by Western blotting.Results: Among TRIM proteins, TRIM6 expression was significantly elevated in LUAD tissues. The prognosis analysis demonstrated that high expression of TRIM6 was associated with unfavorable survival, which was consistent with the findings of Cox regression analysis. Further correlation analysis concluded that high TRIM6 expression was also associated with TNM staging. TRIM6 knockdown suppressed proliferation, induced cell apoptosis and cell cycle arrest in the G2/M phase. Furthermore, the exact effect of TRIM6 on LUAD cells was examined using in vivo experiments. Mechanistically, TRIM6 enhanced the biological capacity of LUAD cells through the p53 signaling pathway.Conclusion: Our study identifies TRIM6 is a potential oncogene and a prognostic target through the regulation of p53 signaling pathway in LUAD. 
651 4 |a United States--US 
651 4 |a China 
653 |a Software 
653 |a Medical prognosis 
653 |a Metastasis 
653 |a Regression analysis 
653 |a Lung cancer 
653 |a Bioinformatics 
653 |a Cell adhesion & migration 
653 |a Experiments 
653 |a Biomarkers 
653 |a Correlation analysis 
653 |a Colorectal cancer 
653 |a Tumors 
653 |a Genes 
653 |a Apoptosis 
653 |a Cell growth 
653 |a Survival analysis 
653 |a Cell cycle 
653 |a Breast cancer 
653 |a Proteins 
700 1 |a Wang, Haifeng 
700 1 |a Yu, Tingting 
773 0 |t International Journal of General Medicine  |g vol. 18 (2025), p. 2107 
786 0 |d ProQuest  |t Health & Medical Collection 
856 4 1 |3 Citation/Abstract  |u https://www.proquest.com/docview/3190895342/abstract/embedded/7BTGNMKEMPT1V9Z2?source=fedsrch 
856 4 0 |3 Full Text + Graphics  |u https://www.proquest.com/docview/3190895342/fulltextwithgraphics/embedded/7BTGNMKEMPT1V9Z2?source=fedsrch 
856 4 0 |3 Full Text - PDF  |u https://www.proquest.com/docview/3190895342/fulltextPDF/embedded/7BTGNMKEMPT1V9Z2?source=fedsrch