Lung Adenocarcinoma

These results suggest a model in which sortilin exhibits potential tumor suppressor-like activity by concurrently binding to regulatory elements of cMYC. Sortilin expression in lung adenocarcinoma may be predictive of the efficacy of anti-EGFR therapies.

Up-regulated MALAT1 subsequently sponged miR-690, leading to its functional depletion, autophagosome-lysosome fusion blockade, and aggravated lipid retention. Collectively, the METTL3-m6A/MALAT1/miR-690 axis orchestrates autophagy and lipid homeostasis, operationalizing an "m6A-long non-coding RNA (lncRNA)-microRNA (miRNA)" regulatory paradigm in NAFLD and offering an epitranscriptomic perspective on disease pathogenesis.

TTF-1 negativity identifies a subset of LUAD with worse outcomes to immunotherapy, chemo-immunotherapy, and KRASG12C inhibitors.

MLKL, associated with necroptosis, plays a crucial role in SCLC progression and may serve as a potential prognostic biomarker.

EGFR 19Del and 21L858R mutations are associated with distinct expression patterns of VEGFR1 and CD34, which may underlie differential responses to anti-angiogenic therapy and inform future combination treatment strategies.

Furthermore, FEN1 is associated with immune microenvironment regulation, and in some cases, may be associated with immunotherapy response. In LIHC models, experimental validation revealed that FEN1 stimulates tumorigenesis by stimulating proliferation, migration, and genomic instability.

In vivo, OSBPL3 silencing significantly attenuated tumor growth and promoted apoptosis. Collectively, these findings identify an OSBPL3-NFE2L2-PLAU-AKT signaling axis that drives glycolytic metabolism and LUAD progression, showing its potential as a therapeutic target.

Our study defines a FOSL1-TCOF1-ribosome axis that promotes CPT tolerance in NSCLC by maintaining HR repair. These findings provide a rationale for targeting ribosome biogenesis to enhance CPT-based treatment and highlight coordinated regulation of transcription, protein synthesis, and DNA repair under chemotherapeutic stress.

Stimulation also induced IL-12, IL-21, and TNF-α secretion, which are cytokines known to enhance antitumor immunity. Overall, the data indicte that CD11c+ TIL-Bs are a potential target for anticancer therapeutic approaches and/or a potential prognostic biomarker for cancer prognosis.

Notably, restoring SCN4B levels suppressed LUAD cell viability, migration and invasion in vitro, accompanied by inhibition of EMT. These findings highlighted SCN4B as a potential tumor suppressor and a promising therapeutic target for LUAD.

Combining Shox2 and Rassf1a methylation with EGFR mutations demonstrated enhanced discriminative capacity for early-stage lesions. Our study demonstrated that comprehensive analysis of methylation and gene mutations could provide a novel clinical strategy for molecular subtyping and precision medicine in LUAD.

These results indicate that the proteomic impact of SIRT3 modulation is strongly influenced by cellular metabolic context. All raw mass spectrometry data are publicly available in PXD063181.