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West Ashley Library
9 a.m. - 7 p.m.
Phone: (843) 766-6635
Folly Beach Library
9 a.m. - 5:30 p.m.
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Edgar Allan Poe/Sullivan's Island Library
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Wando Mount Pleasant Library
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Phone: (843) 805-6888
Village Library
9 a.m. - 6 p.m.
Phone: (843) 884-9741
St. Paul's/Hollywood Library
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Keith Summey North Charleston Library
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KLK6/PAR1 Axis Promotes Tumor Growth and Metastasis by Regulating Cross-Talk between Tumor Cells and Macrophages.
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- Author(s): Hwang, Yo Sep; Cho, Hee Jun; Park, Eun Sun; Lim, Jeewon; Yoon, Hyang Ran; Kim, Jong-Tae; Yoon, Suk Ran; Jung, Haiyoung; Choe, Yong-Kyung; Kim, Yong-Hoon; Lee, Chul-Ho; Kwon, Yong Tae; Kim, Bo Yeon; Lee, Hee Gu
- Source:
Cells (2073-4409); Dec2022, Vol. 11 Issue 24, p4101, 18p- Subject Terms:
- Source:
- Additional Information
- Abstract: Kallikrein-related peptidase (KLK)6 is associated with inflammatory diseases and neoplastic progression. KLK6 is aberrantly expressed in several solid tumors and regulates cancer development, metastatic progression, and drug resistance. However, the function of KLK6 in the tumor microenvironment remains unclear. This study aimed to determine the role of KLK6 in the tumor microenvironment. Here, we uncovered the mechanism underlying KLK6-mediated cross-talk between cancer cells and macrophages. Compared with wild-type mice, KLK6−/− mice showed less tumor growth and metastasis in the B16F10 melanoma and Lewis lung carcinoma (LLC) xenograft model. Mechanistically, KLK6 promoted the secretion of tumor necrosis factor-alpha (TNF-α) from macrophages via the activation of protease-activated receptor-1 (PAR1) in an autocrine manner. TNF-α secreted from macrophages induced the release of the C-X-C motif chemokine ligand 1 (CXCL1) from melanoma and lung carcinoma cells in a paracrine manner. The introduction of recombinant KLK6 protein in KLK6−/− mice rescued the production of TNF-α and CXCL1, tumor growth, and metastasis. Inhibition of PAR1 activity suppressed these malignant phenotypes rescued by rKLK6 in vitro and in vivo. Our findings suggest that KLK6 functions as an important molecular link between macrophages and cancer cells during malignant progression, thereby providing opportunities for therapeutic intervention. [ABSTRACT FROM AUTHOR]
- Abstract: Copyright of Cells (2073-4409) is the property of MDPI and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
- Abstract:
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