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IL-1β Induces Fascin Expression and Increases Cancer Invasion.
Anticancer Res. 2018 Nov; 38(11):6127-6132.AR

Abstract

BACKGROUND/AIM

Tumor microenvironment plays an important role in tumor growth and metastasis. Cancer cells can promote their growth and malignancy by altering the surrounding stroma. Fascin is an actin-bundling protein that regulates the dynamics of the cytoskeletal structure and plays a significant role in cancer invasion and metastasis. In this study, we observed stromal factors controlling fascin expression in cancer cells and investigated underlying signal transduction pathways.

MATERIALS AND METHODS

Fascin depletion was performed with lentiviral short-hairpin RNA (shRNA) against fascin mRNA and a stable cell line (Fascindep) was established. Fascin expression and invasion activity induced by IL-1β treatement were observed through Matrigel-Transwell invasion and 3D culture system. Intermediated signaling molecules involved in fascin expression induced by IL-1β were elucidated using western blotting.

RESULTS

Fascin was more highly expressed in human OSCC cells than normal cells. Cancer invasion activity was decreased by fascin depletion using lentiviral shRNA. However, fascin expression was increased by IL-1β treatement, leading to increased extracellular matrix (ECM) degradation and infiltration into 3-dimensional (3-D) collagen matrix. Specific inhibitors of extracellular signal-regulated kinases-1/2 [ERK1/2, (PD98059)], c-Jun N-terminal kinase [JNK, (SP600125)], nuclear factor kappa light chain enhancer of activted B cells [NF-κB, (parthenolide)], and cAMP response element binding protein [CREB, (CREB inhibitor)] suppressed IL-1β -induced fascin expression. IL-1β induced phosphorylation of ERK1/2, JNK, NF-κB and CREB while IL-1 receptor (IL-1R) antagonist abolished their activation.

CONCLUSION

IL-1β is a critical inducer of fascin expression. ERK1/2, JNK, NF-κB, and CREB signaling pathways are involved in IL-1β-induced fascin expression and these paracrine signaling pathways can induce cancer cell invasion.

Authors+Show Affiliations

Department of Dental Hygiene, College of Health Science, Eulji University, Seongnam, Republic of Korea.Department of Dental Hygiene, College of Health Science, Eulji University, Seongnam, Republic of Korea.Department of Dental Hygiene, College of Health Science, Eulji University, Seongnam, Republic of Korea.Department of Dental Hygiene, College of Health Science, Eulji University, Seongnam, Republic of Korea kiteys@eulji.ac.kr.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

30396928

Citation

Lee, Min Kyeong, et al. "IL-1β Induces Fascin Expression and Increases Cancer Invasion." Anticancer Research, vol. 38, no. 11, 2018, pp. 6127-6132.
Lee MK, Park JH, Gi SH, et al. IL-1β Induces Fascin Expression and Increases Cancer Invasion. Anticancer Res. 2018;38(11):6127-6132.
Lee, M. K., Park, J. H., Gi, S. H., & Hwang, Y. S. (2018). IL-1β Induces Fascin Expression and Increases Cancer Invasion. Anticancer Research, 38(11), 6127-6132. https://doi.org/10.21873/anticanres.12964
Lee MK, et al. IL-1β Induces Fascin Expression and Increases Cancer Invasion. Anticancer Res. 2018;38(11):6127-6132. PubMed PMID: 30396928.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - IL-1β Induces Fascin Expression and Increases Cancer Invasion. AU - Lee,Min Kyeong, AU - Park,Ji Hyeon, AU - Gi,Seol Hwa, AU - Hwang,Young Sun, PY - 2018/09/07/received PY - 2018/09/21/revised PY - 2018/09/28/accepted PY - 2018/11/7/entrez PY - 2018/11/7/pubmed PY - 2018/12/18/medline KW - 3D culture KW - IL-1β KW - antagonist KW - cancer invasion KW - fascin SP - 6127 EP - 6132 JF - Anticancer research JO - Anticancer Res. VL - 38 IS - 11 N2 - BACKGROUND/AIM: Tumor microenvironment plays an important role in tumor growth and metastasis. Cancer cells can promote their growth and malignancy by altering the surrounding stroma. Fascin is an actin-bundling protein that regulates the dynamics of the cytoskeletal structure and plays a significant role in cancer invasion and metastasis. In this study, we observed stromal factors controlling fascin expression in cancer cells and investigated underlying signal transduction pathways. MATERIALS AND METHODS: Fascin depletion was performed with lentiviral short-hairpin RNA (shRNA) against fascin mRNA and a stable cell line (Fascindep) was established. Fascin expression and invasion activity induced by IL-1β treatement were observed through Matrigel-Transwell invasion and 3D culture system. Intermediated signaling molecules involved in fascin expression induced by IL-1β were elucidated using western blotting. RESULTS: Fascin was more highly expressed in human OSCC cells than normal cells. Cancer invasion activity was decreased by fascin depletion using lentiviral shRNA. However, fascin expression was increased by IL-1β treatement, leading to increased extracellular matrix (ECM) degradation and infiltration into 3-dimensional (3-D) collagen matrix. Specific inhibitors of extracellular signal-regulated kinases-1/2 [ERK1/2, (PD98059)], c-Jun N-terminal kinase [JNK, (SP600125)], nuclear factor kappa light chain enhancer of activted B cells [NF-κB, (parthenolide)], and cAMP response element binding protein [CREB, (CREB inhibitor)] suppressed IL-1β -induced fascin expression. IL-1β induced phosphorylation of ERK1/2, JNK, NF-κB and CREB while IL-1 receptor (IL-1R) antagonist abolished their activation. CONCLUSION: IL-1β is a critical inducer of fascin expression. ERK1/2, JNK, NF-κB, and CREB signaling pathways are involved in IL-1β-induced fascin expression and these paracrine signaling pathways can induce cancer cell invasion. SN - 1791-7530 UR - https://www.unboundmedicine.com/medline/citation/30396928/IL_1β_Induces_Fascin_Expression_and_Increases_Cancer_Invasion_ L2 - http://ar.iiarjournals.org/cgi/pmidlookup?view=long&pmid=30396928 DB - PRIME DP - Unbound Medicine ER -