The bidirectional relationship between cilia and PCP signaling pathway core protein Vangl2.

Vangl2, a core component of the PCP signaling pathway, serves as a scaffold protein on the cell membrane, playing a crucial role in organizing protein complexes. Cilia, dynamic structures on the cell surface, carry out a wide range of functions. Research has highlighted a bidirectional regulatory interaction between Vangl2 and cilia, underscoring their interconnected roles in cellular processes.

Dual network analysis of transcriptome data for discovery of new therapeutic targets in non-small cell lung cancer.

The drug therapy for non-small cell lung cancer (NSCLC) have always been issues of poisonous side effect, acquired drug resistance and narrow applicable population. In this study, we built a novel network analysis method (difference- correlation- enrichment- causality- node), which was based on the difference analysis, Spearman correlation network analysis, biological function analysis and Bayesian causality network analysis to discover new therapeutic target of NSCLC in the sequencing data of BEAS-2B and 7 NSCLC cell lines. Our results showed that, as a proteasome subunit coding gene in the central of cell cycle network, PSMD2 was associated with prognosis and was an independent prognostic factor for NSCLC patients.

Targeting STT3A produces an anti-tumor effect in lung adenocarcinoma by blocking the MAPK and PI3K/AKT signaling pathway.

Background: Glycosylation is crucial for the stability and biological functions of proteins. The aberrant glycosylation of critical proteins plays an important role in multiple cancers, including lung adenocarcinoma (LUAD). STT3 oligosaccharyltransferase complex catalytic subunit A (STT3A) is a major isoform of N-linked glycosyltransferase that catalyzes the glycosylation of various proteins.

Identification of GPX4 as a therapeutic target for lung adenocarcinoma after EGFR-TKI resistance.

Background: Tyrosine kinase inhibitor (TKI) treatment has significantly improved the prognosis of oncogenic-driven lung adenocarcinoma (LUAD). However, drug resistance limits the long-term benefits of patients. Therefore, there is a pressing need to explore the mechanism of TKI resistance and identify new therapeutic targets.

Identifies Immune Feature Genes for Prediction of Chemotherapy Benefit in Cancer.

Chemotherapy is still the most fundamental treatment for advanced cancers so far. Previous studies have indicated that immune cell infiltration (ICI) index could serve as a biomarker to predict chemotherapy benefit in breast cancer and colorectal cancer. However, due to different responses of tumor infiltrating immune cells (TIICs) to chemotherapy, the prediction efficiency of ICI index is not fully confirmed by now.

Decreased expression of EFCC1 and its prognostic value in lung adenocarcinoma.

Background: So far, there is a lack of reliable prognostic biomarkers for lung adenocarcinoma (ADC). Initially, we found that EF-hand and coiled-coil domain containing 1 (EFCC1) was a novel gene which was downregulated consistently with the progression of lung ADC in The Cancer Genome Atlas (TCGA) data through bioinformatics analysis. In this study, we aimed to evaluate the prognostic significance of EFCC1 in lung ADC in both TCGA data and clinical samples.

Formylated honokiol analogs showed antitumor activity against lung carcinoma.

Honokiol, a biphenolic neolignan with inappreciable toxicity isolated from Magnolia officinalis, has been reported to have antiangiogenic and antitumor properties in several tumor cell lines and tumor xenograft models. In our previous study, structural modification by chemical synthesis has been carried out to develop novel honokiol derivatives to improve antitumor activity and clarify the structure-activity relationship. Honokiol analogs, especially 3,5'-diformylated honokiol HK-(CHO)2, have been found to moderately block the newly grown segmental vessels from the dorsal aorta in the transgenic zebrafish-based assay, show antiangiogenic property, and exert medium cytotoxicity against two lung cell lines (Lewis lung carcinoma LL/2 cells and human non-small-cell lung cancer A549 cells).

Metformin synergistically sensitizes FLT3-ITD-positive acute myeloid leukemia to sorafenib by promoting mTOR-mediated apoptosis and autophagy.

Mutations of Fms-like tyrosine kinase 3-internal tandem duplication (FLT3-ITD), accounting for approximately 30% of patients with acute myeloid leukemia (AML), results in poor therapeutic efficacy and short survival. Sorafenib, an oral multikinase inhibitor, can inhibit FLT3 and improve clinical outcome of FLT3 mutated leukemia. Our current studies have shown that, the antidiabetic drug metformin also exerts anti-leukemic effect by activating p-AMPK and synergistically sensitizes FLT3 mutated AML to sorafenib.