scholarly journals HIF‐1α is necessary for activation and tumour‐promotion effect of cancer‐associated fibroblasts in lung cancer

2021 ◽  
Author(s):  
Yana Zhang ◽  
Yangyang Bian ◽  
Yuan Wang ◽  
Yuanyuan Wang ◽  
Xixi Duan ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Associated Fibroblasts ◽  
Promotion Effect ◽  
Tumour Promotion

scholarly journals Gas6 derived from cancer-associated fibroblasts promotes migration of Axl-expressing lung cancer cells during chemotherapy

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Ryu Kanzaki ◽  
Hisamichi Naito ◽  
Kazuyoshi Kise ◽  
Kazuhiro Takara ◽  
Daisuke Eino ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Lung Cancer Cells ◽  
Cancer Associated Fibroblasts

scholarly journals Cancer-Associated Fibroblasts Accelerate Malignant Progression of Non-Small Cell Lung Cancer via Connexin 43-Formed Unidirectional Gap Junctional Intercellular Communication

2018 ◽  
Vol 51 (1) ◽  
pp. 315-336 ◽  
Author(s):  
Min Luo ◽  
Yanmei Luo ◽  
Naiquan Mao ◽  
Guolin Huang ◽  
Cuifang Teng ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Intercellular Communication ◽  
Connexin 43 ◽  
Small Cell ◽  
Migration And Invasion ◽  
Cancer Associated Fibroblasts ◽  
Gap Junctional Intercellular Communication ◽  
Small Cell Lung ◽  
Metabolic Coupling ◽  
Gap Junctional

Background/Aims: Gap junctions, which are assembled by connexins, can directly connect the cytoplasm of adjacent cells and enable gap junctional intercellular communication (GJIC) as well as metabolic coupling between neighboring cells. Here, we investigated the role of connexin 43 (Cx43) and its derived GJIC in the interplay between non-small cell lung cancer (NSCLC) cells and cancer-associated fibroblasts (CAFs). Methods: CAFs and NSCLC cells were co-cultured with direct contact and separated using flow cytometry. Glucose uptake, lactate production, and the expression and activity of PKM-2 and LDH-A in sorted CAFs were measured by a colorimetric assay, western blotting, and enzyme-linked immunosorbent assay (ELISA). Meanwhile, E-cadherin and N-cadherin expression and the migration and invasion of sorted NSCLC cells were detected by western blotting, wound width, and Transwell assays. Pyruvate, acetyl-CoA, and citric acid levels, ATP levels, and LDH-B and α-KG activity in sorted NSCLC cells were determined by a colorimetric or fluorometric assay and ELISA, respectively. Functional GJIC between cells and the subcellular location of connexins were detected by a “Parachute” assay and immunofluorescence. Levels of α-SMA, Cx43, and LDH-B in tissue from patients with NSCLC were determined by immunohistochemistry. Results: Cx43 accumulated in the plasma membrane, which favored the assembly of asymmetric unidirectional GJIC from CAFs to NSCLC cells. CAFs underwent increased aerobic glycolysis and promoted the epithelial-mesenchymal transition, migration, and invasion of NSCLC cells. In contrast, NSCLC cells experienced enhanced oxidative phosphorylation upon CAF stimulation, with an increase in ATP generation and thereby activation of the PI3K/Akt and MAPK/ERK pathways. Metabolic coupling between CAFs and NSCLC cells was under the strict control of Cx43-formed unidirectional GJIC. Patients with high tri-expression of α-SMA, Cx43, and LDH-B had the shortest overall survival and relapse-free survival compared with those with individual overexpression or high bi-expression. Conclusion: Cx43-formed unidirectional GJIC plays a critical role in mediating close metabolic cooperation between CAFs and NSCLC cells to support the malignant progression of NSCLC.

scholarly journals miR-200 deficiency promotes lung cancer metastasis by activating cancer-associated fibroblasts

2020 ◽  
Author(s):  
Bin Xue ◽  
Chen-Hua Chuang ◽  
Haydn M. Prosser ◽  
Cesar Seigi Fuziwara ◽  
Claudia Chan ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Lung Adenocarcinoma ◽  
Cancer Cells ◽  
Molecular Mechanisms ◽  
Cancer Metastasis ◽  
Lung Cancer Mortality ◽  
Tumor Stroma ◽  
Metastatic Potential ◽  
Human Lung Cancer ◽  
Cancer Associated Fibroblasts

AbstractLung adenocarcinoma, the most prevalent lung cancer subtype, is characterized by its high propensity to metastasize. Despite the importance of metastasis in lung cancer mortality, its underlying cellular and molecular mechanisms remain largely elusive. Here, we identified miR-200 miRNAs as potent suppressors for lung adenocarcinoma metastasis. miR-200 expression is specifically repressed in mouse metastatic lung adenocarcinomas, and miR-200 decrease strongly correlates with poor patient survival. Consistently, deletion of mir-200c/141 in the KrasLSL-G12D/+; Trp53flox/flox lung adenocarcinoma mouse model significantly promoted metastasis, generating a desmoplastic tumor stroma highly reminiscent of metastatic human lung cancer. miR-200 deficiency in lung cancer cells promotes the proliferation and activation of adjacent cancer-associated fibroblasts (CAFs), which in turn elevates the metastatic potential of cancer cells. miR-200 regulates the functional interaction between cancer cells and CAFs, at least in part, by targeting Notch ligand Jagged1 and Jagged2 in cancer cells and inducing Notch activation in adjacent CAFs. Hence, the interaction between cancer cells and CAFs constitutes an essential mechanism to promote metastatic potential.

scholarly journals New relationship of E2F1 and BNIP3 with caveolin‐1 in lung cancer‐associated fibroblasts

2020 ◽  
Vol 11 (6) ◽  
pp. 1369-1371
Author(s):  
Cheng Shen ◽  
Xuanming Chen ◽  
Kai Xiao ◽  
Guowei Che
Keyword(s):  
Lung Cancer ◽  
Cancer Associated Fibroblasts ◽  
Caveolin 1 ◽  
Relationship Of

scholarly journals Metabolic Alterations in Lung Cancer–Associated Fibroblasts Correlated with Increased Glycolytic Metabolism of the Tumor

2013 ◽  
Vol 11 (6) ◽  
pp. 579-592 ◽  
Author(s):  
Virendra K. Chaudhri ◽  
Gregory G. Salzler ◽  
Salihah A. Dick ◽  
Melanie S. Buckman ◽  
Raffaella Sordella ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Associated Fibroblasts ◽  
Glycolytic Metabolism ◽  
Metabolic Alterations
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