Lung cancer (LC) is considered to have the highest mortality rate around the world. Because there are no early diagnostic signs or efficient clinical alternatives, distal metastasis and increasing numbers of recurrences are a challenge in the clinical management of LC. Long non-coding RNAs (lncRNAs) have recently been recognized as a critical regulator involved in the progression and treatment response to LC. The Wnt/β-catenin pathway has been shown to influence LC occurrence and progress. Therefore, discovering connections between Wnt signaling pathway and lncRNAs may offer new therapeutic targets for improving LC treatment and management. In this review, the purpose of this article is to present possible therapeutic approaches by reviewing particular relationships, key processes, and molecules associated to the beginning and development of LC.

Protein glycation is an important protein post-translational modification and is one of the main pathogenesis of diabetic angiopathy. Other than glycated hemoglobin, the protein glycation of other globins such as myoglobin (Mb) is less studied. The protein glycation of human Mb with ribose has not been reported, and the glycation sites in the Mb remain unknown. This article reports that d-ribose undergoes rapid protein glycation of human myoglobin (HMb) at lysine residues (K34, K87, K56, and K147) on the protein surface, as identified by ultra-high performance liquid chromatography-mass spectrometry (UHPLC-MS) and electrospray ionization tandem mass spectrometry (ESI-MS/MS). Moreover, glycation by d-ribose at these sites slightly decreased the rate of the met heme (Fe^III) in reaction with H₂O₂ to form a ferryl heme (Fe^IV=O). This study provides valuable insight into the protein glycation by d-ribose and provides a foundation for studying the structure and function of glycated heme proteins.

Lung cancer recently has been documented as the leading cause of cancer-related mortality, posing a severe burden on global public health. Nowadays, immunotherapy—particularly programmed cell death 1 (PD-1)/programmed death-ligand 1 (PD-L1) targeted immune checkpoint inhibitors (ICIs)—offers promising options for the clinical treatment of non-small cell lung cancer (NSCLC). However, treatment failure following immune checkpoint inhibitor therapy is frequently observed in patients with NSCLC. Surprisingly, mitochondria, the core hub for cellular metabolism and signal transduction, play a critical role in ICI resistance. Mounting evidence indicates that mitochondrial functional dynamics modulate PD-L1 expression and further govern tumor immune evasion via multiple pathways. Notably, metabolic and immunological differences exist among distinct lung cancer subtypes. This review systematically summarizes the mechanisms of mitochondrial regulation of PD-L1 expression in NSCLC, the differences in this regulation across lung cancer subtypes, and provides novel agents for developing mitochondria-targeted combination immunotherapy for the treatment of patients. We also highlight key outstanding questions to guide future research in this field.

Background: Lung adenocarcinoma (LUAD), the most prevalent histological subtype of lung cancer, remains a leading cause of cancer-related mortality due to late diagnosis, metastasis, and therapy resistance. The aim of the study is to investigate the role of Kinetochore Scaffold 1 (KNL1) in promoting LUAD progression and its underlying molecular regulatory mechanisms. Methods: KNL1 mRNA expression levels across 33 cancer types were analyzed using bioinformatics analysis based on the TCGA database. Immunohistochemistry (IHC) was used to assess KNL1 expression in LUAD and normal tissues. Stable KNL1-knockdown and KNL1-overexpressing LUAD cell lines were established using lentiviral infection. Western blotting (WB) was used to measure epithelial-mesenchymal transition (EMT) markers and ferroptosis-related protein expression. Cell migration was evaluated via scratch wound healing assays. The thiobarbituric acid (TBA) method was employed for the detection of malondialdehyde. a fluorescent probe was utilized to determine ferrous ion content. WB determined the phosphorylation ratios of AMP-activated protein kinase (AMPK) and mammalian target of rapamycin (mTOR) proteins. Results: 1. KNL1 was highly expressed in 31 cancer types, including LUAD. Kaplan-Meier curves showed significantly shorter median survival in patients with high KNL1 expression. IHC confirmed upregulated KNL1 expression in LUAD tissues. 2. KNL1 overexpression significantly promoted LUAD cell migration and increased mesenchymal marker expression, whereas KNL1 knockdown exerted opposite effects. 3. KNL1 overexpression significantly reduced MDA content and Fe2+ levels in RSL3-treated LUAD cells while increasing the expression of key ferroptosis defense proteins; conversely, it markedly increased the accumulation of MDA and Fe2+ and downregulated these proteins. KNL1 overexpression significantly increased phosphorylated AMPK (p-AMPK) expression but decreased phosphorylated mTOR (p-mTOR) expression in RSL3-treated LUAD cells; conversely, it inhibited p-AMPK expression and activated p-mTOR. Conclusion: KNL1 promotes lung adenocarcinoma progression by suppressing ferroptosis through regulation of the AMPK-mTOR signaling pathway.