期刊
BONE
卷 144, 期 -, 页码 -出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.bone.2020.115829
关键词
PTCH1; Anchorage-independent growth; Invasion; Bone metastasis; Lung cancer
资金
- Basic Science Research Program through the National Research Foundation of Korea (NRF) - Ministry of Education and Science Technology (MEST) [2016R1E1A1A0191433, 2019R1I1A1A01061544]
- Grant of the Samsung Medical Center [OTC1190111]
- National Cancer Center (NCC) [194154]
- National Research Foundation of Korea [2019R1I1A1A01061544] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
The study investigates the role of PTCH1 in bone metastasis and suggests that PTCH1 may be an important regulator of cancer cell invasion. Knockdown of PTCH1 decreases anchorage-independent growth and metastatic potential of non-small cell lung cancer cells.
Acquisition of metastatic potential by cancer cells is related to cancer stemness and anchorage-independent growth. The onset and progression of cancer are known to involve Hedgehog (HH) signaling that is activated by the binding of HH to the Patched 1 (PTCH1) receptor. However, the functions and mechanisms of action of PTCH1 in the context of bone metastasis remain to be elucidated. In this study, lentivirally-delivered shRNA was used to deplete PTCH1 levels, which resulted in the inhibition of spherical colony formation by the human non-small cell lung cancer (NSCLC) cell line; this suggested that PTCH1 promotes anchorage-independent growth. Concordantly, knockdown of PTCH1 resulted in significantly reduced migration and invasion of NSCLC cells; this was accompanied by the downregulation of MMP7 and SOX2. PTCH1 knockdown resulted in decreased bone destruction and osteoclastogenesis in a mouse bone metastasis model. These results indicate that PTCH1 may be an important regulator of bone invasion, and strongly suggest that knockdown of PTCH1 may decrease the anchorage-independent growth and metastatic potential of NSCLC.
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