Enhanced cell motility and invasion of chicken embryo fibroblasts in response toJUN over-expression

Bos, Timothy J.; Margiotta, Patricia; Bush, Linnette; Wasilenko, William J.

doi:10.1002/(sici)1097-0215(19990505)81:3<404::aid-ijc14>3.0.co;2-i

Cited by 29 publications

(6 citation statements)

References 16 publications

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“…Similarly, AP-1 has been reported to be overexpressed in different neoplastic cells and can also closely regulate the hallmarks of carcinogenesis [37,74,75]. Several AP-1 target genes, such as matrix metalloproteinases [MMPs] (MMP-1, MMP-3 and MMP-9), extracellular matrix associated proteins, and protein kinase C, have been implicated in carcinogenesis [76,77,78]. Furthermore, AP-1 has also been found to interact with NF-κB and augment cancer progression [38,79,80].…”

Section: Introductionmentioning

confidence: 99%

Fangchinoline, a Bisbenzylisoquinoline Alkaloid can Modulate Cytokine-Impelled Apoptosis via the Dual Regulation of NF-κB and AP-1 Pathways

et al. 2019

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Fangchinoline (FCN) derived from Stephaniae tetrandrine S. Moore can be employed to treat fever, inflammation, rheumatism arthralgia, edema, dysuria, athlete’s foot, and swollen wet sores. FCN can exhibit a plethora of anti-neoplastic effects although its precise mode of action still remains to be deciphered. Nuclear factor-κB (NF-κB) and activator protein-1 (AP-1) can closely regulate carcinogenesis and thus we analyzed the possible action of FCN may have on these two signaling cascades in tumor cells. The effect of FCN on NF-κB and AP-1 signaling cascades and its downstream functions was deciphered using diverse assays in both human chronic myeloid leukemia (KBM5) and multiple myeloma (U266). FCN attenuated growth of both leukemic and multiple myeloma cells and repressed NF-κB, and AP-1 activation through diverse mechanisms, including attenuation of phosphorylation of IκB kinase (IKK) and p65. Furthermore, FCN could also cause significant enhancement in TNFα-driven apoptosis as studied by various molecular techniques. Thus, FCN may exhibit potent anti-neoplastic effects by affecting diverse oncogenic pathways and may be employed as pro-apoptotic agent against various malignancies.

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Section: Introductionmentioning

confidence: 99%

Fangchinoline, a Bisbenzylisoquinoline Alkaloid can Modulate Cytokine-Impelled Apoptosis via the Dual Regulation of NF-κB and AP-1 Pathways

et al. 2019

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“…C-Jun/AP-1 also directly stimulates effectors of metastasis such as ezrin and MMP9 through specifically binding to their promoters [ 38 , 39 ]. Ezrin shares a sequence homology with the 4.1 proteins; however, it has been recognized as a pro-metastatic factor.…”

Section: Discussionmentioning

confidence: 99%

Protein 4.1N acts as a potential tumor suppressor linking PP1 to JNK-c-Jun pathway regulation in NSCLC

Wang

et al. 2015

Oncotarget

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Protein 4.1N is a member of protein 4.1 family and has been recognized as a potential tumor suppressor in solid tumors. Here, we aimed to investigate the role and mechanisms of 4.1N in non-small cell lung cancer (NSCLC). We confirmed that the expression level of 4.1N was inversely correlated with the metastatic properties of NSCLC cell lines and histological grade of clinical NSCLC tissues. Specific knockdown of 4.1N promoted tumor cell proliferation, migration and adhesion in vitro, and tumor growth and metastasis in mouse xenograft models. Furthermore, we identified PP1 as a novel 4.1N-interacting molecule, and the FERM domain of 4.1N mediated the interaction between 4.1N and PP1. Further, ectopic expression of 4.1N could inactivate JNK-c-Jun signaling pathway through enhancing PP1 activity and interaction between PP1 and p-JNK. Correspondingly, expression of potential downstream metastasis targets (ezrin and MMP9) and cell cycle targets (p53, p21 and p19) of JNK-c-Jun pathway were also regulated by 4.1N. Our data suggest that down-regulation of 4.1N expression is a critical step for NSCLC development and that repression of JNK-c-Jun signaling through PP1 is one of the key anti-tumor mechanisms of 4.1N.

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“…Several genes known to be regulated by AP-1 were highly expressed in our samples, including EGFR , MMP3 and MMP9 . [8, 36]. …”

Section: Discussionmentioning

confidence: 99%

“…The human primary chondrosarcoma cell lines JJ and KC [8], the human primary chordoma cell line, the human metastatic chordoma cell line [27] and the human melanoma cell line Colo 38 were grown at 37°C in a 5% CO 2 atmosphere in RPMI 1640 medium supplemented with 10% fetal calf serum (BioWhittaker, Walkersville, MD).…”

Section: Methodsmentioning

confidence: 99%

Chordoma and chondrosarcoma gene profile: implications for immunotherapy

Schwab

Boland

Agaram

et al. 2008

Cancer Immunol Immunother

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Chordoma and chondrosarcoma are malignant bone tumors characterized by the abundant production of extracellular matrix. The resistance of these tumors to conventional therapeutic modalities has prompted us to delineate the gene expression profile of these two tumor types, with the expectation to identify potential molecular therapeutic targets. Furthermore the transcriptional profile of chordomas and chrondrosarcomas was compared to a wide variety of sarcomas as well as to that of normal tissues of similar lineage, to determine whether they express unique gene signatures among other tumors of mesenchymal origin, and to identify changes associated with malignant transformation. A HG-U133A Affymetrix Chip platform was used to determine the gene expression signature in 6 chordoma and 14 chondrosarcoma lesions. Validation of selected genes was performed by qPCR and immunohistochemistry (IHC) on an extended subset of tumors. By unsupervised clustering, chordoma and chondrosarcoma tumors grouped together in a genomic cluster distinct from that of other sarcoma types. They shared overexpression of many extracellular matrix genes including aggrecan, type II & X collagen, fibronectin, matrillin 3, high molecular weight-melanoma associated antigen (HMW-MAA), matrix metalloproteinase MMP-9, and MMP-19. In contrast, T Brachyury and CD24 were selectively expressed in chordomas, as were Keratin 8,13,15,18 and 19. Chondrosarcomas are distinguished by high expression of type IX and XI collagen. Because of its potential usefulness as a target for immunotherapy, the expression of HMW-MAA was analyzed by IHC and was detected in 62% of chordomas and 48% of chondrosarcomas, respectively. Furthermore, western blotting analysis showed that HMW-MAA synthesized by chordoma cell lines has a structure similar to that of the antigen synthesized by melanoma cells. In conclusion, chordomas and chondrosarcomas share a similar gene expression profile of up-regulated extracellular matrix genes. HMW-MAA represents a potential useful target to apply immunotherapy to these tumors.

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Enhanced cell motility and invasion of chicken embryo fibroblasts in response toJUN over-expression

Cited by 29 publications

References 16 publications

Fangchinoline, a Bisbenzylisoquinoline Alkaloid can Modulate Cytokine-Impelled Apoptosis via the Dual Regulation of NF-κB and AP-1 Pathways

Fangchinoline, a Bisbenzylisoquinoline Alkaloid can Modulate Cytokine-Impelled Apoptosis via the Dual Regulation of NF-κB and AP-1 Pathways

Protein 4.1N acts as a potential tumor suppressor linking PP1 to JNK-c-Jun pathway regulation in NSCLC

Chordoma and chondrosarcoma gene profile: implications for immunotherapy

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