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M. Jiang
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P2.01 - Poster Session with Presenters Present (ID 461)
- Event: WCLC 2016
- Type: Poster Presenters Present
- Track: Biology/Pathology
- Presentations: 1
- Moderators:
- Coordinates: 12/06/2016, 14:30 - 15:45, Hall B (Poster Area)
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P2.01-010 - Downregulation of PFTK1 by shRNA Inhibits Migration and Invasion of Human Non-Small Cell Lung Cancer Cell Lines (ID 3776)
14:30 - 14:30 | Author(s): M. Jiang
- Abstract
Background:
PFTK1, a novel cyclin-dependent kinases, plays pivotal roles in cell proliferation, differentiation and cell cycle regulation. It has been reported that cell motility and invasiveness could be enhanced by PFTK1 in kinds of tumors. However, the function of PFTK1 in NSCLC metastasis is not clear. The aim of this study was to explore the potential role of PFTK1 in NSCLC metastasis.
Methods:
Expression of protein PFTK1 was assessed by immunohistochemistry staining in tissue microarrays, containing paired tumor tissue and adjacent NSCLC tissue from 119 cases of human lung cancer. PFTK1 was knocked down by shRNA interference method both in human H1299 and 95C cells. Then we applied H1299 and 95C cells that PFTK1 expression was inhibited into the next study. The effect of PFTK1 on cell migration and invasion was explored by cell wound healing assay and transwell assay. Western blot was used to detect whether PFTK1 influences the expression of EMT related proteins β-catenin, vimentin and ZEB1. Cytoskeleton preotein F-actin was observed using cell immunofluorescence test.
Results:
Immunohistochemistry staining of 119 NSCLC patients showed that a high level of PFTK1 expression was correlated with lymph node metastasis and T stage(P<0.05). And detailed analysis indicated that the high expression of PFTK1 was associated with poor prognosis for NSCLC patients (P<0.05). In addition, suppression of PFTK1 inhibited cell migration and invasion in H1299 and 95C cells. Inhibition of PFTK1 decreased the expression of β-catenin, vimentin, as well as ZEB1. Cytoskeletal protein F-actin was also decreased by the down-regulation of PFTK1.
Conclusion:
We reported for the first time that PFTK1 was overexpressed in samples of NSCLC. The high expression of PFTK1 was associated with lymph node metastasis, T stage and poor prognosis for NSCLC patients. Furthermore, our data indicated that PFTK1 promoted cells migration and invasion by regulating the expression of cytoskeletal protein F-actin and modulating EMT events. Therefore, our findings suggest that PFTK1 would be a potential target to development of therapies for NSCLC.
