Lung cancer, the leading cause of death worldwide, is associated with the highest morbidity. Non-small cell lung cancer (NSCLC) accounts for 80–85% of lung cancer cases. Advances in the domain of cancer treatment have improved the prognosis and quality of life of patients with metastatic NSCLC. Nevertheless, tumor progression or metastasis owing to treatment failure caused by primary or secondary drug resistance remains the cause of death in the majority of cases. Epithelial–mesenchymal transition (EMT), a vital biological process wherein epithelial cancer cells lose their inherent adhesion and transform into more invasive mesenchymal-like cells, acts as a powerful engine driving tumor metastasis. EMT can also induce immunosuppression in the tumor environment, thereby promoting cancer development and poor prognosis among patients with NSCLC. This review aims to elucidate the effect of EMT on metastasis and the tumor immune microenvironment. Furthermore, it explores the possible roles of EMT inhibition in improving the treatment efficacy of NSCLC. Targeting EMT may be an ideal mechanism to inhibit tumor growth and progression at multiple steps.

With the extensive use of immune checkpoint inhibitors (ICI) in advanced-stage cancers, immune-related adverse events (irAEs) have been noted in various systems. While most irAEs are reversible and manageable, cardiac toxicities are rare but life-threatening, with high mortality rates. We present a case of a 71-year-old man with cholangiocarcinoma who developed myocarditis related to ICIs 29 days after the first infusion of teriprizumab combined with albumin-bound paclitaxel and gemcitabine. He was initially asymptomatic after admission but with substantial elevations of troponin I and myocardial enzymes. Sixteen hours after admission, he developed palpitations, dizziness, and syncope. Electrocardiography confirmed third-degree atrioventricular block and frequent ventricular premature contractions for which he received high-dose corticosteroids and a permanent pacemaker. The patient survived and permanently discontinued immunotherapy. Early identification and intervention are the keys to improving the prognosis of immune myocarditis.

This study was aimed at exploring the mechanism of serine threonine protein kinase 11 (STK11)/Adenosine 5 ^′‐monophosphate‐activated protein kinase (AMPK) signaling pathway after immunotherapy for esophageal squamous cell carcinoma (ESCC), providing basic information for the clinical treatment of ESCC. In this study, tissue specimens from 100 patients with ESCC who underwent surgical treatment in Taizhou People’s Hospital (group A) and 20 patients with recurrent or metastatic ESCC who received second‐line immunotherapy (group B) were collected. The real‐time fluorescent quantitative polymerase chain reaction (PCR) (RT‐qPCR) technology was used to detect the expression levels of STK11, interferon‐γ (IFN‐γ), interleukin 6 (IL‐6), and vascular endothelial growth factor (VEGF) in the tissues. The immunohistochemical staining was used to detect the positive expression levels (PELs) of STK11 and AMPKα in the tissues, and immunofluorescence staining was used to detect the PELs Teff cells (CD3 and CD8), Treg cells (CD4 and FOXP3), and neutrophils (CD68 and CD163). RT‐qPCR results showed that the expression levels of STK11 and IFN‐γ in group A were obviously lower, and those of IL‐6 and VEGF were much higher in contrast to group B (P < 0.05). The results of immunohistochemical staining showed that the number of STK11‐ and AMPKα‐positive staining cells in group A was dramatically less than that in group B (P <0.05). The results of immunofluorescence staining revealed that the number of positive staining cells for Teff cells, Treg cells, and neutrophils in group A was also less dramatically than that in group B (P <0.05). In summary, immunotherapy can play a therapeutic effect on ESCC by regulating STK11/AMPK pathway and immune cell infiltration.

This study aimed to investigate the effects of radiation (RT) on protein and protein S-palmitoylation levels in esophageal cancer (EC) cell lines. EC cells (N = 6) were randomly divided into RT and negative control. The results revealed that 592 proteins were identified in the RT group, including 326 upregulation proteins and 266 downregulation proteins. These differentially expressed proteins were involved in cellular biological processes. S-palmitoylation sequencing analysis revealed that 830 and 899 S-palmitoylation cysteine sites were upregulated and downregulated, respectively. Differential S-palmitoylation proteins were primarily found in cellular processes, anatomical entities, and binding activities. Kyoto encyclopedia of genes and genomes (KEGG) pathway and protein-protein interaction analysis revealed that differential S-palmitoylation proteins are involved in proteoglycans in cancer, shigellosis, EGFR tyrosine kinase inhibitor resistance, nucleocytoplasmic transport, and mineral absorption. In conclusion, this study demonstrated that RT significantly affects protein expression and S-palmitoylation levels in EC cell lines, which has implications for cancer biology-related cellular processes and pathways. These findings enhance understanding of the molecular mechanisms underlying the response of EC cells to RT treatment.