Tumor-associated macrophages (TAMs) play a critical role in modulating the tumor microenvironment and promote tumor metastases. Our studies have demonstrated that ginsenoside Rh2 (G-Rh2), a monomeric compound extracted from ginseng, is a promising anti-tumor agent in lung cancer cells. However, it remains unclear whetherG-Rh2 can modulate the differentiation of TAMs and its interaction with tumor microenvironment. In this study, we investigated how G-Rh2 regulates the phenotype of macrophages and affects the migration of non-small cell lung cancer (NSCLC) cells. Murine macrophage-like RAW264.7 cells and human THP-1 monocyte were differentiated into M1 and M2 subsets of macrophages with different cytokines combination, which were further identified by flow cytometry with specific biomarkers. M2 macrophages were sorted out to co-culture with NSCLC cell lines, A549 and H1299. Wound healing assay was performed to examine the cell migration. Expression levels of matrix metalloproteinases 2 and 9 (MMP-2, − 9) and vascular endothelial growth factor-C (VEGF-C) were measured by RT-qPCR and western blot, and the release of VEGF in the supernatant was measured by a VEGF ELISA kit. Finally, modulation of TAMs phenotype and VEGF expression by G-Rh2 was examined in vivo. We demonstrated that M2 subset of macrophages alternatively differentiated from RAW264.7 or THP-1cells promote migration of NSCLC cells. Further examinations revealed that NSCLC significantly increased the release of VEGF to the media and elevated the expression levels of VEGF at mRNA and protein levels after being co-cultured with M2 macrophages. Similar alterations in MMP-2 and MMP-9 were observed in NSCLC after being co-cultured. Of note,G-Rh2 had a potential to effectively convert M2 phenotype to M1 subset of macrophages. Importantly, G-Rh2 had a preference to decrease the expression levels of VEGF, MMP2, and MMP9 in co-cultured lung cancer cells, over than those in lung cancer cells without co-culturing. Consistently, G-Rh2 reduced M2 macrophage marker CD206 and VEGF expression levels in vivo. All of these results suggested that M2 subset macrophages drive lung cancer cells with more aggressive phenotypes. G-Rh2 has a potential to convert TAMs from M2 subset to M1 in the microenvironment and prevents lung cancer cell migration, suggesting the therapeutic effects of G-Rh2onlung cancer.

Purpose: To evaluate the role of DSCC1 in LUAD. Patients and Methods: Based on TCGA and GTEx, the Wilcoxon rank-sum test was used to compare the expression differences of DSCC1 between the normal samples of GTEx combined TCGA and the unpaired tumor samples of TCGA, and to compare DSCC1 expression values between tumor tissues and paired normal LUAD tissues in the TCGA cohort. Kruskal–Wallis rank-sum test, Wilcoxon rank-sum test, and logistics regression were used to compare the relationship between the expression of DSCC1 and the clinicopathological parameters. The biological function of DSCC1 was annotated by GSEA and ssGSEA, while Kaplan–Meier and Cox regression analysis were used to evaluate the prognostic value of DSCC1. Furthermore, the time-dependent ROC curve was used to analyze the diagnostic efficacy of DSCC1 in LUAD. Results: We downloaded the RNA-Seq data of 513 LUAD cases. The expression of DSCC1 was significantly correlated with T stage (OR = 1.04(1.02– 1.07), P = 0.002), pathological stage (OR=1.03 (1.01– 1.05), P = 0.008) and TP53 status (OR=1.10 (1.07– 1.14), P < 0.001). The high expression of DSCC1 was significantly correlated with DSS (HR=1.56 (1.07– 2.26), P = 0.021) and OS (HR=1.53 (1.14– 2.05), P = 0.004). Moreover, ROC curve analysis (AUC=0.845, CI (0.820-0.870)) indicated DSCC1 as a potential diagnostic molecule for LUAD. In the group with high DSCC1 expression phenotype, down-regulation of EGFR signal, reduction of IL-6 deprivation, cell cycle, and p53 signal pathway were significantly abundant. Spearman correlation analysis showed that the expression of DSCC1 was positively correlated with the infiltration of Th2 cells, T Helper cells. Conclusion: Our results suggest that DSCC1 may be an important biomarker for the treatment of LUAD.

Background Recent years have witnessed growing interest in the interplay between B cells and non-small cell lung cancer (NSCLC) amid deepening investigations into cancer immunotherapy. B cells play pivotal roles in immunotherapeutic contexts by modulating tumor progression through immunoglobulin secretion, T-cell response activation, and direct tumoricidal activity. In this study, we employ bibliometric techniques to analyze research hotspots and evolutionary trends in NSCLC-associated B-cell investigations, aiming to inform future directions in this burgeoning field. Methods We conducted a systematic retrieval of peer-reviewed documents (original articles, reviews, editorials) from the Web of Science Core Collection (2004–2024). Bibliometric networks were constructed using CiteSpace 6.1.R6 and VOSviewer 1.6.18. With temporal productivity patterns analyzed through Microsoft Excel 2021. Results This study analyzed 437 publications from 1,677 institutions across 156 countries/regions, encompassing 3,360 researchers. Annual publications showed sustained growth (2004–2021) followed by decline (2022–2024). China demonstrated highest productivity (n = 169), the United States dominated total citations (6,943). Keyword and highly cited literature analyses primarily focused on elucidating B cell heterogeneity and tertiary lymphoid structures, deciphering B cell-T cell interaction mechanisms, and exploring synergistic applications of B cells with other immunotherapeutic approaches. Conclusion This study utilizes bibliometric analysis to explore research hotspots and developmental trends in B - cell - related studies of non - small cell lung cancer (NSCLC) over the past two decades. By elucidating the changing research landscape, this work aims to enhance researchers’ comprehension of the immunological milieu and advancements in NSCLC immunotherapy, promote scientific advancement in this field, and provide directional guidance for future research.

Background and purpose: Esophageal cancer has the seventh highest incidence and sixth highest fatality rate of all malignant tumors. It’s a type of cancer that has a greater fatality rate than morbidity. In the treatment of advanced esophageal and squamous cell carcinoma, targeted and immune checkpoint inhibitors have showed promising outcomes in recent years. The aim of this research was to examine the effectiveness and safety of immune checkpoint inhibitors in combination with antiangiogenic medicines in the treatment of unresectable patients with locally progressed / distant metastatic esophageal squamous cell carcinoma. Methods: Before April 15, 2022, randomized controlled trials of immune checkpoint inhibitors combined with anti-angiogenic drugs in the treatment of esophageal cancer will be searched on PubMed, Cochrane Library, EMBASE, WebofScience, China Knowledge Network, Wanfang Data Knowledge Service Platform, and VIP. The two authors independently extracted the data, checked the data, and used the “bias risk” tool in the Cochrane intervention system evaluation manual to independently evaluate the bias included in the study. When the extracted data were similar enough, the Revman5.4 software was used for meta analysis. If the summary data could not be collected for meta analysis, the results would be summarized in a narrative way. Discussion: This paper introduces in detail the systematic review and design method of immune checkpoint inhibitors mixture with antiangiogenic drugs in the treatment of unresectable locally advanced / distant metastatic esophageal squamous cell carcinoma. Systematic review registration: The review protocol has been registered in PROSPERO CRD42022324666