E-cigarette promotes breast carcinoma progression and lung metastasis: Macrophage-tumor cells crosstalk and the role of CCL5 and VCAM-1

Pham, Kien; Huynh, Do Luong; Le, Le; Delitto, Daniel; Yang, Lei; Huang, Jing; Kang, Yibin; Steinberg, Michael B.; Li, Jieliang; Zhang, Lanjing; Liu, Dongfang; Tang, Moon‐shong; Liu, Chen; Wang, He

doi:10.1016/j.canlet.2020.08.010

Cited by 30 publications

(11 citation statements)

References 55 publications

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“…Lung metastases were also significantly more frequent among rodents from the exposure group. The same research clearly confirmed the increase of the capability of pathologic cells to escape apoptosis after exposure to e-cigarette vapor [46]. Based on these observations, it was assumed that vaping was associated with tumor progression as well as with a limitation of the immune response, which enabled destruction of cancer cells shortly after their implantation.…”

Section: Influence On Carcinogenesissupporting

confidence: 56%

Potential Benefits and Hazards Associated with the Use of E-Cigarettes—A Guide for Practitioners and Current Status in Poland

Kruszewski

Worobiej

Kolasińska

et al. 2021

Advances in Respiratory Medicine

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Section: Influence On Carcinogenesissupporting

confidence: 56%

Potential Benefits and Hazards Associated with the Use of E-Cigarettes—A Guide for Practitioners and Current Status in Poland

Kruszewski

Worobiej

Kolasińska

et al. 2021

Advances in Respiratory Medicine

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“…CAFs are a heterogeneous population; however, HSCs with high ACTA2 and FAP mRNA expression levels activated by adjacent tumor cells are considered to be the main source of CAFs in HCC ( 29 ). In the TME, infiltrated monocytes or resident macrophages are recruited by several factors, such as CCL5 and TGF-β, and form a diverse spectrum of TAMs, which are the main regulators of tumor-related inflammation ( 30 , 31 ). TAMs are mainly divided into two different polarization types.…”

Section: Discussionmentioning

confidence: 99%

Cancer‑associated fibroblast‑induced M2‑polarized macrophages promote hepatocellular carcinoma progression via the plasminogen activator inhibitor‑1 pathway

et al. 2021

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Targeting the tumor stroma is an important strategy in cancer treatment. Cancer-associated fibroblasts (CAFs) and tumor-associated macrophages (TAMs) are two main components in the tumor microenvironment (TME) in hepatocellular carcinoma (HCC), which can promote tumor progression. Plasminogen activator inhibitor-1 (PAI-1) upregulation in HCC is predictive of unfavorable tumor behavior and prognosis. However, the crosstalk between cancer cells, TAMs and CAFs, and the functions of PAI-1 in HCC remain to be fully investigated. In the present study, macrophage polarization and key paracrine factors were assessed during their interactions with CAFs and cancer cells. Cell proliferation, wound healing and Transwell and Matrigel assays were used to investigate the malignant behavior of HCC cells in vitro. It was found that cancer cells and CAFs induced the M2 polarization of TAMs by upregulating the mRNA expression levels of CD163 and CD206, and downregulating IL-6 mRNA expression and secretion in the macrophages. Both TAMs derived from cancer cells and CAFs promoted HCC cell proliferation and invasion. Furthermore, PAI-1 expression was upregulated in TAMs after being stimulated with CAF-conditioned medium and promoted the malignant behavior of the HCC cells by mediating epithelial-mesenchymal transition. CAFs were the main producer of C-X-C motif chemokine ligand 12 (CXCL12) in the TME and CXCL12 contributed to the induction of PAI-1 secretion in TAMs. In conclusion, the results of the present study suggested that CAFs promoted the M2 polarization of macrophages and induced PAI-1 secretion via CXCL12. Furthermore, it was found that PAI-1 produced by the TAMs enhanced the malignant behavior of the HCC cells. Therefore, these factors may be targets for inhibiting the crosstalk between tumor cells, CAFs and TAMs.

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“…A previous study suggested that CD80 binds to the CTLA-4 receptor, inhibiting T-cell activation [44]. TAMs could independently stimulate tumor cell growth and migration via theCCL5/CCR1/CCR5 axis [45]. These ndings revealed that FANCD2 plays a crucial role in recruiting different TIICs and regulating anti-tumor immunity.…”

Section: Discussionmentioning

confidence: 90%

Upregulation of Ferroptosis-Related Fanconi Anemia Group D2 is a Poor Prognostic Factor and Indicator of Tumor Immune Cell Infiltration in Lung Adenocarcinoma

Zhang

Wang

Chen

et al. 2022

Preprint

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Background: Fanconi anemia (FA) group D2 (FANCD2) is a ferroptosis-related gene crucial for DNA damage repair and negatively regulates ferroptosis. Our study aimed to evaluate its prognostic value as well as its association with ferroptosis and immune infiltration in lung adenocarcinoma (LUAD). Methods: Transcriptome sequencing data and clinical information, three independent cohorts, as well as immunohistochemistry, were collected from the TCGA, GEO, and HPA databases, respectively. Univariate and multivariate analyses were used to assess the correlations between FANCD2 expression and overall survival or clinicopathological parameters. cBioPortal was utilized to investigate the FANCD2 alteration status. Gene and protein networks based on FANCD2 interactions were generated using GeneMANIA and STRING, respectively. Based on the CancerSEA database, the function of FANCD2 was explored at the single-cell level. The relationships between FANCD2 expression levels and tumor-infiltrating immune cells and their equivalent gene signatures were analyzed by TIMER, GEPIA, TISIDB, and ssGSEA databases. CIBERSORT was used to analyze the relevance of the infiltration of 24 types of immune cells. Results: The results revealed that FANCD2 expression was significantly upregulated in LUAD and lung squamous cell carcinoma (LUSC) tissues than in normal tissues. Further, the overexpression of FANCD2 was closely associated with poor survival for LUAD patients but not for LUSC patients. FANCD2 expression levels were related to tumor-infiltrating immune cells and their matching gene signatures, including CD8+ T cells, NK cells, DC cells, and Th2 cells in cases of LUAD. Conclusion: FANCD2 was identified as a crucial molecule underlying the synergistic effects of ferroptosis and immunotherapy for LUAD patients.

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E-cigarette promotes breast carcinoma progression and lung metastasis: Macrophage-tumor cells crosstalk and the role of CCL5 and VCAM-1

Cited by 30 publications

References 55 publications

Potential Benefits and Hazards Associated with the Use of E-Cigarettes—A Guide for Practitioners and Current Status in Poland

Potential Benefits and Hazards Associated with the Use of E-Cigarettes—A Guide for Practitioners and Current Status in Poland

Cancer‑associated fibroblast‑induced M2‑polarized macrophages promote hepatocellular carcinoma progression via the plasminogen activator inhibitor‑1 pathway

Upregulation of Ferroptosis-Related Fanconi Anemia Group D2 is a Poor Prognostic Factor and Indicator of Tumor Immune Cell Infiltration in Lung Adenocarcinoma

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