RBM15-dependent m6A modification mediates progression of non-small cell lung cancer cells DOI Creative Commons
Man Wang,

Ya‐Zhen Qin,

Xiaoqi Ai

et al.

Molecular Medicine, Journal Year: 2024, Volume and Issue: 30(1)

Published: Dec. 23, 2024

Non-small cell lung cancer (NSCLC) is the predominant form of cancer, contributing significantly to global health and economic challenges. This study elucidated role RBM15 in NSCLC progression through its involvement m6A modifications. levels tissues cells were assessed via RT-qPCR Western blotting. The impact knockdown on proliferation, invasion, migration was evaluated using CCK-8, colony formation, Transwell assays. Expression KLF1, TRIM13, ANXA8 determined by blot. methylation analyzed, while RIP MeRIP assays employed explore interaction between YTHDF1/YTHDF2/m6A KLF1/TRIM13, as well KLF1 binding promoter. ubiquitination examined Xenograft metastasis models utilized assess RBM15's vivo. found be overexpressed NSCLC. Silencing led decreased cells. upregulated downregulated TRIM13 YTHDF1/YTHDF2, resulting promotion expression. overexpression or downregulation partially reversed suppressive effects proliferation. ANXA8, NSCLC, mitigated inhibitory silencing malignant behaviors. In vivo, hindered proliferation modulating KLF1-TRIM13/ANXA8 axis. RBM15-mediated enhances expression suppresses thereby promoting facilitating progression. These findings provide novel insights potential therapeutic targets for treatment.

Language: Английский

The interaction between m6A modification and noncoding RNA in tumor microenvironment on cancer progression DOI

Liushan Wei,

Shun Liu, Zhizhong Xie

et al.

International Immunopharmacology, Journal Year: 2024, Volume and Issue: 140, P. 112824 - 112824

Published: Aug. 7, 2024

Language: Английский

Citations

1
Effect of Annexin A2 on prognosis and sensitivity to immune checkpoint plus tyrosine kinase inhibition in metastatic renal cell carcinoma DOI Creative Commons
Jiajun Wang, Jinglai Lin, Jiahao Wang

et al.

Discover Oncology, Journal Year: 2024, Volume and Issue: 15(1)

Published: March 22, 2024

Abstract Background Immunotherapy (IO) plus tyrosine kinase inhibitor (TKI) therapy is the first-line recommendation for advanced renal cell carcinoma (RCC), but no biomarker has been approved it. Annexin A2 (ANXA2) can induce immune escape in tumors. Methods Two independent cohorts of RCC treated by IO + TKI were utilized survival analysis (ZS-MRCC, n = 45; Javelin-101, 726). ANXA2 expression was determined RNA-sequencing. The impact on tumor microenvironment assessed RNA-sequencing, flow cytometry and immunohistochemistry two localized datasets (ZS-HRRCC, 40; TCGA-KIRC, 530). Results upregulated non-responders (p 0.027). High-ANXA2 group showed poor progression-free (PFS) both ZS-MRCC cohort (HR, 2.348; 95% CI 1.084–5.085; P 0.025) Javelin-101 1.472; 1.043–2.077; Multivariate Cox regression as an prognostic factor 2.619; 1.194–5.746; 0.016). correlated with decreased proportion granzyme B CD8 T cells (Spearman’s ρ − 0.40, 0.01), increased TIM-3 0.43, < 0.001) CTLA4 0.49, tumor-infiltrating lymphocytes. A random forest (RF) score further build integrating genes, which stratified patients who would benefit from (low-RF score, vs TKI, HR 0.453, 0.328–0.626; high-RF 0.877, 0.661–1.165; interaction 0.003). Conclusions Upregulated associated PFS therapeutic resistance therapy, related exhaustion. integrated RF could stratify therapy.

Language: Английский

Citations

0
Exploring the Therapeutic Potential of β-Hydroxybutyrate (BHB) in Clear Cell Renal Cell Carcinoma: A Journey into Fat Browning, Autophagy, and Tumor Slimming DOI Creative Commons
Roya Rezaei, Asra Abdali Larki, Rosa Hosseinzadegan

et al.

International Journal of Clinical Practice, Journal Year: 2024, Volume and Issue: 2024, P. 1 - 13

Published: May 15, 2024

This study delves into the therapeutic potential of β-hydroxybutyrate (BHB) in clear cell renal carcinoma (ccRCC), a cancer known for its complex pathogenesis and resistance to conventional treatments. The research specifically explores impact BHB on viability, autophagy induction, lipid metabolism Caki-1 cells. findings reveal that significantly reduces ccRCC particularly under low-glucose conditions. combination glucose treatment activates pathways, as evidenced by increased expression autophagy-related genes (Beclin-1, LC3IIβ, ATG5) decreased P62 after 48 72 hours. Moreover, combined therapy enhances metabolism, indicated elevated PGC-1α UCP-1, along with upregulation ACSL3 CPT1A, which are associated droplet formation facilitate breakdown within concludes holds promise agent ccRCC, targeting abnormal inducing autophagy-mediated death, promoting fat browning. results suggest avenues precision-guided nutritional therapies treatment, highlighting innovative role addressing challenges posed this cancer.

Language: Английский

Citations

0
Identification of diagnostic markers and molecular clusters of cuproptosis-related genes in alcohol-related liver disease based on machine learning and experimental validation DOI Creative Commons
Jiangfa Li, Yong Wang, Zhan Wu

et al.

Heliyon, Journal Year: 2024, Volume and Issue: 10(18), P. e37612 - e37612

Published: Sept. 1, 2024

Language: Английский

Citations

0
RBM15-dependent m6A modification mediates progression of non-small cell lung cancer cells DOI Creative Commons
Man Wang,

Ya‐Zhen Qin,

Xiaoqi Ai

et al.

Molecular Medicine, Journal Year: 2024, Volume and Issue: 30(1)

Published: Dec. 23, 2024

Non-small cell lung cancer (NSCLC) is the predominant form of cancer, contributing significantly to global health and economic challenges. This study elucidated role RBM15 in NSCLC progression through its involvement m6A modifications. levels tissues cells were assessed via RT-qPCR Western blotting. The impact knockdown on proliferation, invasion, migration was evaluated using CCK-8, colony formation, Transwell assays. Expression KLF1, TRIM13, ANXA8 determined by blot. methylation analyzed, while RIP MeRIP assays employed explore interaction between YTHDF1/YTHDF2/m6A KLF1/TRIM13, as well KLF1 binding promoter. ubiquitination examined Xenograft metastasis models utilized assess RBM15's vivo. found be overexpressed NSCLC. Silencing led decreased cells. upregulated downregulated TRIM13 YTHDF1/YTHDF2, resulting promotion expression. overexpression or downregulation partially reversed suppressive effects proliferation. ANXA8, NSCLC, mitigated inhibitory silencing malignant behaviors. In vivo, hindered proliferation modulating KLF1-TRIM13/ANXA8 axis. RBM15-mediated enhances expression suppresses thereby promoting facilitating progression. These findings provide novel insights potential therapeutic targets for treatment.

Language: Английский

Citations

0