Serum CD166: A novel biomarker for predicting nasopharyngeal carcinoma response to radiotherapy

Huan, Lin; Chen, Ze-Tan; Zhu, Xiao‐Dong; Li, Ling; Qu, Song; Zhao, Wei; Su, Fang; Wei, Jing-Ni; Liang, Zhong‐Guo; Mo, Qi-Yan; Wu, Jiang-Bo; Meng, Han

doi:10.18632/oncotarget.16399

Cited by 10 publications

(8 citation statements)

References 39 publications

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“…All experiments were conducted three times. Dose–response curves were analyzed using the multitarget single-hit model in the GraphPad Prism 5.0 software 13 , 14 with the formula: Survival fraction (SF)=1 − (1 − e − D / D 0 ) N , where D 0 (mean lethal dose) is the single dose of radiation that kills 63% of cells, N represents the number of intracellular radiosensitive areas; Dq (lnN * D 0 ) is the required threshold for cell damage. When the Dq increases, the survival curve area is widened, and radioresistance is increased.…”

Section: Methodsmentioning

confidence: 99%

The role of autophagy in the radiosensitivity of the radioresistant human nasopharyngeal carcinoma cell line CNE-2R

Liang¹,

Lin²,

Yu³

et al. 2018

CMAR

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PurposeThe present study aimed to study the role of autophagy in the radiosensitivity of the radioresistant human nasopharyngeal carcinoma cell line CNE-2R.MethodsBefore being irradiated, CNE-2R cells were treated with the autophagy inhibitor chloroquine diphosphate (CDP) or the autophagy inducer rapamycin (RAPA). Microtubule-associated protein light chain 3 (LC3-II) and p62 were assessed using Western blotting analysis 48 hours after CNE-2R cells were irradiated. The percentage of apoptotic cells was assessed via flow cytometry. CNE-2R cell viability was evaluated using the Cell Counting Kit-8 (CCK8). The radiosensitivity of cells was assessed via clone formation analysis.ResultsThe level of autophagy in CNE-2R cells improved as the radiation dose increased, reaching the maximum at a dose of 10 Gy. Autophagy was most significantly inhibited by 60 µmol/L CDP in CNE-2R cells, but was obviously enhanced by 100 nmol/L RAPA. Compared with the irradiation (IR) alone group, in the IR + CDP group, autophagy was significantly inhibited, viability was low, the rate of radiation-induced apoptosis was increased, and radiosensitivity was upregulated. In contrast, cells of the IR + RAPA group exhibited greater autophagy, higher viability, a lower rate of radiation-induced apoptosis, and downregulated radiosensitivity.ConclusionThe autophagy level is negatively correlated with radiosensitivity for the radio-resistant human nasopharyngeal carcinoma cell line CNE-2R.

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Section: Methodsmentioning

confidence: 99%

The role of autophagy in the radiosensitivity of the radioresistant human nasopharyngeal carcinoma cell line CNE-2R

Liang¹,

Lin²,

Yu³

et al. 2018

CMAR

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“…The serum level of CD166/ALCAM in patients with radiation-resistant tumors was higher than that of radiation-sensitive patients; at the cell membrane level, it has been proven that CNE-2 and CNE-2R cells with high expression of CD166/ALCAM had a lower radio-sensitivity than those of CNE-2 and CNE-2R with negative expression. In addition, the expression of CD166/ALCAM was correlated with the radio-sensitivity of NPC 14. In the present study, we applied lentivirus-mediated shRNA to downregulate CD166/ALCAM in CNE-2R cell line.…”

Section: Discussionmentioning

confidence: 80%

“…Our research group identified differentially secreted proteins in the cultured NPC radio-resistant cell line CNE-2R and its parental cell line CNE-2 by proteomics-related identification technique in vitro. Besides, CD166 is positively expressed in CNE-2R, while is negatively expressed in CNE-2; higher expression could also be observed in patients’ serum being radio-resistant NPC than that in radiation-sensitive patients;13 we found that the sensitivity of radiation of NPC cells with positive expression of CD166 is not comparable to that of NPC cells with negative expression 14. It is suggested that the expression of CD166 in the cell membrane is associated with radio-sensitivity of NPC cells.…”

Section: Introductionmentioning

confidence: 66%

<p>Downregulation of CD166 inhibits invasion, migration, and EMT in the radio-resistant human nasopharyngeal carcinoma cell line CNE-2R</p>

Sun

Huan

et al. 2019

CMAR

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Objective: 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.

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“…Radiotherapy is a mainly treatment for nasopharyngeal carcinoma (NPC). However, radioresistance is one of the major factors to affect the therapeutic efficacy and prognosis of patients [1–3]. Accordingly, identifying potential biomarkers and studying the molecular mechanisms associated with radioresistant nasopharyngeal carcinoma has become a hot topic both in basic and clinical research.…”

Section: Introductionmentioning

confidence: 99%

Comprehensive analysis of key genes and microRNAs in radioresistant nasopharyngeal carcinoma

Guo

Zhang

Zhang³

et al. 2019

BMC Med Genomics

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Background Radioresistance is one of the main obstacle limiting the therapeutic efficacy and prognosis of patients, the molecular mechanisms of radioresistance is still unclear. The purpose of this study was to identify the key genes and miRNAs and to explore their potential molecular mechanisms in radioresistant nasopharyngeal carcinoma. Methods In this study, we analysis the differentially expressed genes and microRNA based on the database of GSE48501 and GSE48502, and then employed bioinformatics to analyze the pathways and GO terms in which DEGs and DEMS target genes are involved. Moreover, Construction of protein-protein interaction network and identification of hub genes. Finally, analyzed the biological networks for validated target gene of hub miRNAs. Results A total of 373 differentially expressed genes (DEGs) and 14 differentially expressed microRNAs (DEMs) were screened out. The up-regulated gene JUN was overlap both in DEGs and publicly available studies, which was potentially targeted by three miRNAs, including hsa-miR-203, hsa-miR-24 and hsa-miR-31. Moreover, Pathway analysis showed that both up-regulated gene and DEMs target genes were enriched in TGF-beta signaling pathway, Hepatitis B, Pathways in cancer and p53 signaling pathway. Finally, we further constructed protein-protein interaction network (PPI) of DEGs and analyzed the biological networks for above mentioned common miRNAs, the result indicated that JUN was a core hub gene in PPI network, hsa-miR-24 and its target gene were significantly enriched in P53 signaling pathway. Conclusions These results might provide new clues to improve the radiosensitivity of Nasopharyngeal Carcinoma. Electronic supplementary material The online version of this article (10.1186/s12920-019-0507-6) contains supplementary material, which is available to authorized users.

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Serum CD166: A novel biomarker for predicting nasopharyngeal carcinoma response to radiotherapy

Cited by 10 publications

References 39 publications

The role of autophagy in the radiosensitivity of the radioresistant human nasopharyngeal carcinoma cell line CNE-2R

The role of autophagy in the radiosensitivity of the radioresistant human nasopharyngeal carcinoma cell line CNE-2R

<p>Downregulation of CD166 inhibits invasion, migration, and EMT in the radio-resistant human nasopharyngeal carcinoma cell line CNE-2R</p>

Comprehensive analysis of key genes and microRNAs in radioresistant nasopharyngeal carcinoma

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