Reactive Oxygen Species: Friends or Foes of Lung Cancer?

Guha, Deblina; Banerjee, Shruti; Mukherjee, Shravanti; Dutta, Apratim; Das, Tanya

doi:10.1007/978-981-32-9366-3_14

Cited by 2 publications

(3 citation statements)

References 145 publications

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“…These alterations can lead to treatment resistance by promoting the transdifferentiation of LUAD to squamous cell carcinoma ( 36 , 37 ). However, ROS directly cause cell injury, including DNA damage ( 38 , 39 ). Cancer cells must counteract excessive oxidative damage for survival ( 38 , 39 ).…”

Section: Discussionmentioning

confidence: 99%

“…However, ROS directly cause cell injury, including DNA damage ( 38 , 39 ). Cancer cells must counteract excessive oxidative damage for survival ( 38 , 39 ). Once the DNA is damaged, enzymatic DNA repair mechanisms are activated to maintain genomic stability and cell viability ( 38 , 39 ).…”

Section: Discussionmentioning

confidence: 99%

“…Cancer cells must counteract excessive oxidative damage for survival ( 38 , 39 ). Once the DNA is damaged, enzymatic DNA repair mechanisms are activated to maintain genomic stability and cell viability ( 38 , 39 ). This may explain why ‘DNA_REPAIR’ was identified as another significantly enriched gene set.…”

Section: Discussionmentioning

confidence: 99%

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MRPL51 is a downstream target of FOXM1 in promoting the malignant behaviors of lung adenocarcinoma

Zhang

et al. 2023

Oncol Lett

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Mitochondrial ribosome protein L51 (MRPL51) is a 39S subunit protein of the mitochondrial ribosome. Its dysregulation may be involved in non-small cell lung cancer. The present study aimed to explore MRPL51 expression in lung adenocarcinoma (LUAD) and normal lung tissues, as well as its regulatory effects on malignant LUAD behaviors. In addition, the role of forkhead box protein M1 (FOXM1) in MRPL51 transcription was studied. Bioinformatics analysis and subsequent in vitro experiments, including western blotting, immunofluorescent staining, Transwell invasion assay, dual-luciferase assay and chromatin immunoprecipitation quantitative PCR were conducted. The results demonstrated that MRPL51 expression was upregulated at both the mRNA and protein levels in LUAD tissues compared with normal lung tissues. Gene Set Enrichment Analysis demonstrated that LUAD tissues with higher MRPL51 expression also had higher expression levels of genes enriched in multiple gene sets, including ‘DNA_REPAIR’, ‘UNFOLDED_PROTEIN_RESPONSE’, ‘MYC_TARGETS_V1’, ‘OXIDATIVE_ PHOSPHORYLATION’, ‘MTORC1_SIGNALING’, ‘REACTIVE_OXYGEN_SPECIES_PATHWAY’, ‘MYC_ TARGETS_V2’, ‘E2F_TARGETS’ and ‘G2M_ CHECKPOINT’. MRPL51 expression was positively correlated with ‘cell cycle’, ‘DNA damage’, ‘DNA repair’, epithelial-mesenchymal transition (‘EMT’), ‘invasion’ and ‘proliferation’ of LUAD cells at the single-cell level. Compared to the negative control, MRPL51 knockdown decreased N-cadherin and vimentin expression but increased E-cadherin expression in A549 and Calu-3 cells. MRPL51 knockdown suppressed cell proliferation, induced G1 phase arrest and decreased cell invasion. Patients with LUAD and higher MRPL51 expression had a significantly shorter overall survival (OS). FOXM1 could bind to the MRPL51 gene promoter and activate its transcription. In conclusion, MRPL51 was transcriptionally activated by FOXM1 in LUAD and contributed to the malignant behaviors of tumor cells, including EMT, cell cycle progression and invasion. High MRPL51 expression may be a prognostic biomarker indicating poor OS.

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