Cyclophilin B promotes cell proliferation, migration, invasion and angiogenesis via regulating the STAT3 pathway in non-small cell lung cancer

Teng, Mao-rong; Huang, Jianan; Zhu, Zhengtai; Li, Hua; Shen, Jiangfeng; Chen, Quan

doi:10.1016/j.prp.2019.04.009

Cited by 16 publications

(12 citation statements)

References 25 publications

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“…Meanwhile, CypB downregulation also decreased cell migration and invasion in vitro and inhibited lung and liver metastasis in immunodeficiency mice. It is proved in many studies that CypB protected tumor cells from stress-induced apoptosis mostly through activation of STAT3 signaling pathway [14,15,30,32]. Similarly in this study, co-localization of CypB with STAT3 in nuclei of cell were detected in CRC cell lines in response to IL-6 treatment, which is typical stimulator for activation of STAT3.…”

Section: Discussionsupporting

confidence: 77%

“…Recent studies have suggested that Cyclophilin B (CypB) overexpression is crucial in supporting the activation of STAT3 in tumors [12][13][14][15][16]. CypB is an endoplasmic reticulum (ER)-resident protein with peptidyl-prolyl cis/trans-isomerase activity (PPIase) [17], which belongs to a conserved protein family Cyclophilin, expressed ubiquitously in prokaryotic and eukaryotic organisms [18].…”

Section: Introductionmentioning

confidence: 99%

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High-fat diet induced cyclophilin B enhances STAT3/lncRNA-PVT1 feedforward loop and promotes growth and metastasis in colorectal cancer

et al. 2022

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High-fat diet (HFD) has been implicated to promote colorectal cancer (CRC). Recently, oncogene Cyclophilin B (CypB) is reported to be induced by cholesterol. However, the role of CypB in CRC carcinogenesis and metastasis associated with HFD remains unknown. In the present study, we showed that HFD-induced CypB enhances proliferation and metastasis through an inflammation-driven circuit, including Signal Transducer and Activator of Transcription 3 (STAT3)-triggered transcription of lncRNA-PVT1, and its binding with CypB that promotes activation of STAT3. CypB was found to be upregulated in CRC, which was correlated with elevated body mass index and poor prognosis. HFD induced CypB expression and proinflammatory cytokines in colon of mice. Besides, CypB restoration facilitated growth, invasion and metastasis in CRC cells both in vitro and in vivo. Moreover, RIP sequencing data identified lncRNA-PVT1 as a functional binding partner of CypB. Mechanistically, PVT1 increased the phosphorylation and nuclear translocation of STAT3 in response to IL-6, through directly interaction with CypB, which impedes the binding of Suppressors Of Cytokine Signalling 3 (SOCS3) to STAT3. Furthermore, STAT3 in turn activated PVT1 transcription through binding to its promoter, forming a regulatory loop. Finally, this CypB/STAT3/PVT1 axis was verified in TCGA datasets and CRC tissue arrays. Our data revealed that CypB linked HFD and CRC malignancy by enhancing the CypB/STAT3/PVT1 feedforward axis and activation of STAT3.

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Section: Discussionsupporting

confidence: 77%

Section: Introductionmentioning

confidence: 99%

High-fat diet induced cyclophilin B enhances STAT3/lncRNA-PVT1 feedforward loop and promotes growth and metastasis in colorectal cancer

et al. 2022

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“…Ablation of CypB expression in glioblastoma multiforme cells suppresses several canonical oncogenic signaling pathways, including mutant P53, MYC, and CHK1. Teng and colleagues revealed that CypB was overexpressed in NSCLC and inhibition of CypB could suppress cell proliferation, migration, invasion, and angiogenesis via regulating the STAT3 pathway [ 37 ]. Notably, angiogenesis plays an important role in tumor progression.…”

Section: Discussionmentioning

confidence: 99%

CypB promotes cell proliferation and metastasis in endometrial carcinoma

Liu

Zuo

et al. 2021

BMC Cancer

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Background The molecular pathogenesis of endometrial cancer is not completely understood. CypB upregulated in many cancers, however, its role in endometrial carcinoma has not been studied. Here, we determine the effect of CypB on the growth of endometrial cancer. Methods In this study, we examined the expression of CypB in endometrial cancer tissues using immunohistochemistry. CypB silenced in HEC-1-B cell line by shRNA. CCK-8, colony formation assays, wound healing assays, and transwell analysis were performed to assess its effect on tumor cell proliferation and metastasis. Furthermore, microarray analysis was carried out to compare the global mRNA expression profile between the HEC-1-B and CypB-silenced HEC-1-B cells. Gene ontology and KEGG pathway enrichment analysis were performed to determine the potential function of differentially expressed genes related to CypB. Results We found that CypB was upregulated in endometrial cancer, inhibit CypB expression could significantly suppress cell proliferation, metastasis, and migration. We identified 1536 differentially expressed genes related to CypB (onefold change, p < 0.05), among which 652 genes were upregulated and 884 genes were downregulated. The genes with significant difference in top were mainly enriched in the cell cycle, glycosphingolipid biosynthesis, adherens junctions, and metabolism pathways. Conclusion The results of our study suggest that CypB may serve as a novel regulator of endometrial cell proliferation and metastasis, thus representing a novel target for gene-targeted endometrial therapy. Trial registration YLYLLS [2018] 008. Registered 27 November 2017.

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“…Teng et al. ( 64 ) showed that Cyp B silencing can significantly inhibit A549 proliferation, reduce expression of the angiogenesis-related proteins VEGF and Ang2, and inhibit the proliferation, migration, invasion and angiogenesis of NSCLC cells by regulating the STAT3 signaling pathway. Tumor-associated calcium signal transducer 2 (trop2) has been confirmed to be associated with tumor proliferation and invasion of NSCLC.…”

Section: Novel Angiogenic Regulators In Lung Cancer Treatmentmentioning

confidence: 99%

Novel Angiogenic Regulators and Anti-Angiogenesis Drugs Targeting Angiogenesis Signaling Pathways: Perspectives for Targeting Angiogenesis in Lung Cancer

Lin

Wang

et al. 2022

Front. Oncol.

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Lung cancer growth is dependent on angiogenesis. In recent years, angiogenesis inhibitors have attracted more and more attention as potential lung cancer treatments. Current anti-angiogenic drugs targeting VEGF or receptor tyrosine kinases mainly inhibit tumor growth by reducing angiogenesis and blocking the energy supply of lung cancer cells. However, these drugs have limited efficiency, raising concerns about limited scope of action and mechanisms of patient resistance to existing drugs. Therefore, current basic research on angiogenic regulators has focused more on screening carcinogenic/anticancer genes, miRNAs, lncRNAs, proteins and other biomolecules capable of regulating the expression of specific targets in angiogenesis signaling pathways. In addition, new uses for existing drugs and new drug delivery systems have received increasing attention. In our article, we analyze the application status and research hotspots of angiogenesis inhibitors in lung cancer treatment as a reference for subsequent mechanistic research and drug development.

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Cyclophilin B promotes cell proliferation, migration, invasion and angiogenesis via regulating the STAT3 pathway in non-small cell lung cancer

Cited by 16 publications

References 25 publications

High-fat diet induced cyclophilin B enhances STAT3/lncRNA-PVT1 feedforward loop and promotes growth and metastasis in colorectal cancer

High-fat diet induced cyclophilin B enhances STAT3/lncRNA-PVT1 feedforward loop and promotes growth and metastasis in colorectal cancer

CypB promotes cell proliferation and metastasis in endometrial carcinoma

Novel Angiogenic Regulators and Anti-Angiogenesis Drugs Targeting Angiogenesis Signaling Pathways: Perspectives for Targeting Angiogenesis in Lung Cancer

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