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Yongchu Sun,1 Huan Lin,1 Song Qu,1,2 Ling Li,1,2 Kaihua Chen,1 Binbin Yu,1,2 Guoxiang Lin,2 Fangzhu Wan,1 Xiaodong Zhu1–31Department of Radiation Oncology, Affiliated Tumor Hospital of Guangxi Medical University, Cancer Institute of Guangxi Zhuang Autonomous Region, Nanning, Guangxi 530021, People’s Republic of China; 2Key Laboratory of Early Prevention and Treatment for Regional High Frequency Tumor, Guangxi Medical University, Ministry of Education, Nanning, Guangxi, People’s Republic of China; 3Department of Oncology, Affiliated Wuming Hospitalof Guangxi Medical University, , Nanning, Guangxi 530019, People’s Republic of ChinaObjective: CD166 is known as a tumor stem cell specific marker, associating with tumor metastasis. The purpose of this study was to further discuss CD166 gene on cell proliferation, invasion, metastasis, and the epithelial-mesenchymal transition (EMT) in CNE-2R cell line of nasopharyngeal carcinoma (NPC).Materials and methods: CNE-2R cells were transfected with lentivirus CD166-shRNA, and quantitative reverse transcription polymerase chain reaction (RT-qPCR), and Western blotting were used to confirm the silencing effects. The wound healing test and transwell test were carried out to assess cell invasive and migratory abilities in vitro. With the establishment of xenograft nude mouse model, Western blotting and immunohistochemistry were undertaken to detect the expression level of E-cadherin, N-cadherin, and vimentin. In vivo metastasis detection was carried out by injecting tumor cells into nude mice via the tail vein.Results: The invasive and migratory abilities of CNE-2R cells were significantly reduced after CD166 was downregulated. In addition, silencing of CD166 of CNE-2R cells increased the expression of E-cadherin, while down-regulated the expression of N-cadherin and vimentin. Immunohistochemistry of tumors showed consistent results with in-situ tumor formation experiment. Additionally, the growth of transplanted tumor was inhibited. In addition, in vivo metastasis test proved that knockdown of CD166 suppressed pulmonary metastasis and liver metastasis according to hematoxylin and eosin (H&E) staining. Expression of E-cadherin increased, while expression of N-cadherin and vimentin decreased, as revealed by Western blotting of metastatic lung tumors.Conclusion: Silencing of CD166 in CNE-2R cells evidently inhibited proliferation, invasion, metastasis, and EMT process in vivo and in vitro.Keywords: nasopharyngeal carcinoma, CD166, metastasis, EMT

Guoxiang Lin,1,2,* Binbin Yu,1,2,* Zhongguo Liang,1,2 Ling Li,1–3 Song Qu,1–3 Kaihua Chen,1,2 Lei Zhou,1,2 Qiteng Lu,1,2 Yongchu Sun,1,2 Xiaodong Zhu1–4 1Department of Radiation Oncology, Affiliated Tumor Hospital of Guangxi Medical University and Cancer Institute of Guangxi Zhuang Autonomous Region, Nanning, Guangxi 530021, People’s Republic of China; 2Guangxi Key Laboratory of Early Prevention and Treatment for Regional High Frequency Tumor, Guangxi Medical University, Nanning, Guangxi 530021, People’s Republic of China; 3Key Laboratory of High-Incidence-Tumor Prevention and Treatment (Guangxi Medical University), Ministry of Education, Nanning, Guangxi 530021, People’s Republic of China; 4Department of Oncology, Affiliated Wuming Hospital of Guangxi Medical University, Nanning, Guangxi 530021, People’s Republic of China *These authors contributed equally to this work Background: Previously, we found that c-jun was highly expressed in radiation-resistant human nasopharyngeal carcinoma cells (CNE-2R) compared with human nasopharyngeal carcinoma cells (CNE-2). Materials and methods: In this study, we first used the scratch assays and transwell assays to detect the migration and invasion of CNE-2R and CNE-2 cells and tested the epithelial mesenchymal transformation (EMT)-related proteins E-cadherin and N-cadherin by Western blot analysis. Subsequently, c-jun was knocked down to establish the effect of c-jun on EMT, migration, and invasion of CNE-2R cells both in vitro and in vivo. Results: A high EMT level, CNE-2R cells were more capable of migration and invasion than CNE-2 cells. Moreover, silencing of c-jun has upregulated the expression of E-cadherin and downregulated N-cadherin in CNE-2R cells, and subsequently the migration and invasion capacity of the cells was decreased. Consistent with in vitro results, in vivo studies indicated that the c-jun silencing reduced pulmonary migration of CNE-2R cells. Immunohistochemistry of lung metastatic tumor tissue showed that E-cadherin was upregulated, and N-cadherin was downregulated. Conclusion: These findings suggest that silencing of c-jun in CNE-2R cells reduces cells migration, invasion, and EMT both in vitro and in vivo. Keywords: nasopharyngeal carcinoma, c-jun, migration, invasion, EMT

The microstructures of peanut cake under five levels of applied pressures are measured using stereo light microscope and Image-pro software. Employing the box-counting method, the fractal dimensions of pore structure of peanut cake are measured and calculated. Result shows that the fractal characteristic of peanut cake is obvious. It is found that applied pressure has a significant effect on the fractal dimension, and its value decreases significantly with the increase of applied pressure. It is concluded that with increasing applied pressure the pore structure is further complicated.