Identification of PSMD11 as a novel cuproptosis- and immune-related prognostic biomarker promoting lung adenocarcinoma progression.

BACKGROUND: Due to the unfavorable prognosis associated with lung adenocarcinoma (LUAD), the development of targeted therapies and immunotherapies is essential. Cuproptosis, an emerging form of regulated cell death, is implicated in mitochondrial metabolism and is induced by copper ions. This study aimed to explore the prognostic value of cuproptosis- and immune-related genes (CIRGs) in LUAD. METHODS: We used The Cancer Genome Atlas database to develop a prognostic prediction model for LUAD patients based on eight CIRGs. Using Cox regression analysis, we determined that the CIRG signature is a reliable, independent prognostic factor. We further identified PSMD11 as a critical CIRG and performed immunohistochemistry to study the protein expression levels of PSMD11 in LUAD tissues. We also investigated the impact of PSMD11 on the biological behavior of lung cancer cell lines. RESULTS: We found that patients with low PSMD11 expression levels displayed an improved prognosis compared with those with high PSMD11 expression levels. Overexpression of PSMD11 enhanced proliferation, migration, invasion, and tumor growth of lung carcinoma cell line A549, while PSMD11 knockdown diminished proliferation, migration, invasion, and tumor growth of lung carcinoma cell line PC9. Additionally, we discovered that PSMD11 expression was positively correlated with the infiltration of myeloid-derived suppressor cells and the increased expression of immunosuppressive molecules. CONCLUSION: These findings suggest that PSMD11 may serve as a valuable prognostic biomarker and therapeutic target for LUAD.

Association of cigarette smoking with oral bacterial microbiota and cardiometabolic health in Chinese adults.

The interplay among cigarette smoking status, oral microbiota, and cardiometabolic health is poorly understood. We aimed to examine the association of cigarette smoking status with oral microbiota and to assess the association of the identified microbial features with cardiometabolic risk factors in a Chinese population. This study included 587 participants within the Central China Cohort, including 111 smokers and 476 non-smokers, and their oral microbiota was profiled by 16S rRNA sequencing. Both oral microbial alpha- and beta-diversity were distinct between smokers and non-smokers (p < 0.05). With adjustment for sociodemographics, alcohol and tea drinking, tooth brushing frequency, and body mass index, the relative abundance of nine genera and 26 pathways, including the genus Megasphaera and two pathways involved in inositol degradation which have potentially adverse effects on cardiometabolic health, was significantly different between two groups (FDR q < 0.20). Multiple microbial features related to cigarette smoking were found to partly mediate the associations of cigarette smoking with serum triglycerides and C-reactive protein levels (p-mediation < 0.05). In conclusion, cigarette smoking status may have impacts on the oral microbial features, which may partially mediate the associations of cigarette smoking and cardiometabolic health.

Interleukin-17D promotes lung cancer progression by inducing tumor-associated macrophage infiltration via the p38 MAPK signaling pathway.

Cancer immunoediting is defined as the integration of the immune system's dual host-protective and tumor-promoting roles, including three phases: elimination, equilibrium, and escape. Immune selective pressure causes tumor cells to lose major histocompatibility complex expression or acquire immunosuppressive gene expression, which promotes tumor immune evasion and tumor progression. Interleukin-17D (IL-17D), a member of the IL-17 family of cytokines, plays an important role in the host defense against infection and inflammation. However, the role of IL-17D in the progression of lung cancer remains unclear. In this study, we found that IL-17D was highly expressed in human lung cancer, and increased IL-17D expression was associated with tumor stage and short overall survival. IL-17D overexpression significantly promoted tumor growth in subcutaneous xenograft mouse models but only slightly affected cell proliferation in vitro. Using flow cytometry, we found that IL-17D overexpression enhances the recruitment of tumor-associated macrophages to the tumor microenvironment. Based on the expression profile of IL17D-overexpressing A549 cells, we found that IL-17D increased the expression levels of macrophage polarization- and recruitment-related genes through the MAPK signaling pathway. Moreover, inhibition of the p38 pathway blocked macrophage infiltration induced by IL-17D. These results suggest that IL-17D regulates the tumor immune microenvironment via the p38 MAPK signaling pathway, highlighting IL-17D as a potential therapeutic target for lung cancer.

[Snacking behaviors of Chinese female adults aged 18 to 49 years old in 2004-2015].

OBJECTIVE: To describe shift in snacking behavior among Chinese female adults aged 18 to 49 years old in 2004-2015, and to analyze the contribution of snacks to energy and nutrients among them. METHODS: The present study used data from "China Health and Nutrition Health" where a multistage stratified cluster design was employed to select a stratified probability sample. A total of 12 523 female participants aged 18-49 years old who participated in surveys conducted in 2004-2015 with completed data of demographic characteristics and dietary measurementswere selectedas subjects. There were 2376, 2149, 2142, 2844 and 3012 subjects in waves of 2004, 2006, 2009, 2011, and 2015, respectively. Multivariate Logistic regression model was used to analyze the relationship between socioeconomic factors and snack consumption. Generalized linear model was used to analyze the energy and nutrient intake of snack consumers and non-snack consumers, as well as the contribution of snacks to energy and nutrients. RESULTS: The consumption rate of snacking for women aged 18 to 49 years old had an increasing trend over time(P<0.05), and the rate was 14.24% in 2015, 3.5 times as high as that in 2004. Participants aged 18 to 29 years old whose snake consumption rates were relatively higher compared to those of other aged groups in general waves; also, female adults from the higher education group, the higher yearly income group, and the higher urbanicity index group, and those with the history of smoking or the alcohol use tended to consumed snacks. The change of the influential factors in relation to the consumption of the participant's snack was observed, and age, income level, education level, living area, and the behavior of smoking and drinking were all important factors of snacking. The daily energy and nutrient intake of female snack consumers aged 18 to 49 years old was higher than that of non-snack consumers. The contribution rate of snacks to energy and nutrients varies significantly between survey years; and the contribution of snacks to energy and main nutrients was more than 20% in 2011. CONCLUSION: Snacks have become an important part of the diet of Chinese women aged 18 to 49 years old. Future health promotion programs should be targeted on nutrition education and intervention to guide a reasonable diet structure.

Spi-B Promotes the Recruitment of Tumor-Associated Macrophages via Enhancing CCL4 Expression in Lung Cancer.

Tumor immune escape plays a critical role in malignant tumor progression and leads to the failure of anticancer immunotherapy. Spi-B, a lymphocyte lineage-specific Ets transcription factor, participates in mesenchymal invasion and favors metastasis in human lung cancer. However, the mechanism through which Spi-B regulates the tumor immune environment has not been elucidated. In this study, we demonstrated that Spi-B enhanced the infiltration of tumor-associated macrophages (TAMs) in the tumor microenvironment using subcutaneous mouse models and clinical samples of human lung cancer. Spi-B overexpression increased the expression of TAM polarization- and recruitment-related genes, including CCL4. Moreover, deleting CCL4 inhibited the ability of Spi-B promoting macrophage infiltration. These data suggest that Spi-B promotes the recruitment of TAMs to the tumor microenvironment via upregulating CCL4 expression, which contributes to the progression of lung cancer.