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Interleukin-22 secreted by cancer-associated fibroblasts regulates the proliferation and metastasis of lung cancer cells via the PI3K-Akt-mTOR signaling pathway.

ABSTRACT: Lung cancer is one of the most common human cancers and is the leading cause of cancer-related mortality. Previous studies have suggested that IL-22 might promote the survival of human lung cancer cells. However, the source of IL-22 and the regulatory mechanism of lung cancer cell proliferation remain unclear. In this study, we found that the expression of IL-22 was upregulated in non-small-cell lung cancer (NSCLC) tumor specimens, as revealed by RT-qPCR analysis. Furthermore, IL-22 was profoundly elevated in cell cultures of primary cancer-associated fibroblasts (CAFs) compared to the levels in cell cultures of normal fibroblasts. Moreover, treatment with the supernatant of CAF cell cultures significantly increased the proliferation, migration and invasion of A549 and H1650 cells but reduced apoptosis via the activation of PI3K-Akt-mTOR signaling, and the application of an anti-IL-22 antibody can partially block the effects induced by the CAF cell culture supernatant. Finally, we also identified a panel of critical genes with differential expression between A549 cells treated with and without IL-22. In summary, our results demonstrate a novel regulatory function of IL-22 secreted by CAFs in NSCLC and provide a potential therapeutic target for treating lung cancer.

SUBMITTER: Li H

PROVIDER: S-EPMC6684901 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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Interleukin-22 secreted by cancer-associated fibroblasts regulates the proliferation and metastasis of lung cancer cells via the PI3K-Akt-mTOR signaling pathway.

Li Hongbo H Zhang Quan Q Wu Qi Q Cui Yayun Y Zhu Hong H Fang Mingming M Zhou Xifa X Sun Zhiqiang Z Yu Jingping J

American journal of translational research 20190715 7

Lung cancer is one of the most common human cancers and is the leading cause of cancer-related mortality. Previous studies have suggested that IL-22 might promote the survival of human lung cancer cells. However, the source of IL-22 and the regulatory mechanism of lung cancer cell proliferation remain unclear. In this study, we found that the expression of IL-22 was upregulated in non-small-cell lung cancer (NSCLC) tumor specimens, as revealed by RT-qPCR analysis. Furthermore, IL-22 was profound ...[more]

PMID: 31396319

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Project description:ObjectiveTCP1 is one of the eight subunits of the TCP1 ring complex (TRiC) or the multi-protein mammalian cytosolic chaperone complex. TRiC participates in protein folding and regulates the expression of multiple signaling proteins and cytoskeletal components in cells. Although the clinical importance of its subunits has been clarified in various carcinomas, the function of TCP1 in ovarian cancer (OC) remains unclear. We aimed to identify the association between the expression of TCP1 and the development of epithelial OC (EOC) and patient prognosis, and explore the underlying mechanisms of TCP1 on the tumor progression of OC cells.MethodsTCP1 protein expression was tested in various ovarian tissues by immunohistochemistry, and the correlation between TCP1 expression and clinical physiologic or pathologic parameters of patients with EOC was analyzed. The relationship between TCP1 expression and the prognosis of patients with OC was investigated and analyzed using the Kaplan-Meier (KM) plotter online database. The expression level of TCP1 was then tested in different OC cell lines by Western blotting. Further, a model using OC cell line A2780 was constructed to study the functions of TCP1 in growth, migration, and invasion of human EOC cells. Finally, the possible regulating signaling pathways were discussed.ResultsTCP1 protein expression in OC or borderline tissues was significantly higher than that in benign ovarian tumors and normal ovarian tissue. The upregulated expression of TCP1 in OC was positively associated with the differentiation grade and FIGO stage of tumors and predicted poor clinical outcomes. Compared with IOSE-80 cells, TCP1 protein was overexpressed in A2780 cells. TCP1 knockdown using shRNA lentivirus inhibited the viability of A2780 cells. Western blotting showed that the phosphatidylinositol-3 kinase (PI3K) signaling pathway was activated in the tumor invasion in EOC driven by TCP1.ConclusionUpregulated TCP1 is correlated with the poor prognosis of patients with OC. The mechanism of cancer progression promoted by TCP1 upregulation may be linked to the activation of the PI3K signaling pathway, and TCP1 may serve as a novel target for the treatment of OC.

Dataset Information

Interleukin-22 secreted by cancer-associated fibroblasts regulates the proliferation and metastasis of lung cancer cells via the PI3K-Akt-mTOR signaling pathway.

Publications

Interleukin-22 secreted by cancer-associated fibroblasts regulates the proliferation and metastasis of lung cancer cells via the PI3K-Akt-mTOR signaling pathway.

Similar Datasets

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