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3 results on '"Zheng, Chuanjun"'

1. Down-Regulated CMTM2 Promotes Epithelial-Mesenchymal Transition in Hepatocellular Carcinoma

Author

Zhang, Shidong, Tian, Run, Bei, Chunhua, Zhang, Huixia, Kong, Juan, Zheng, Chuanjun, Song, Xin, Li, Di, Tan, Hongzhuan, Zhu, Xiaonian, and Tan, Shengkui

Subjects
CMTM2, EMT, metastasis, HCC, OncoTargets and Therapy, digestive system diseases, CMTM family members, Original Research
Abstract

Shidong Zhang,1,* Run Tian,1,* Chunhua Bei,1 Huixia Zhang,1 Juan Kong,1 Chuanjun Zheng,1 Xin Song,1 Di Li,1 Hongzhuan Tan,2 Xiaonian Zhu,1 Shengkui Tan1,2 1Department of Epidemiology and Health Statistics, School of Public Health, Guilin Medical University, Guilin 541199, Guangxi, People’s Republic of China; 2Department of Epidemiology and Health Statistics, School of Public Health, Central South University, Changsha 410005, People’s Republic of China*These authors contributed equally to this workCorrespondence: Shengkui Tan; Xiaonian Zhu Email sktan2008@163.com; zhuxiaonian0403@163.comBackground: Our recent study identified that human chemokine-like factor (CKLF)-like MARVEL transmembrane domain-containing family member 2 (CMTM2) was deregulated in hepatocellular carcinoma (HCC) tissues and posed as a potential tumor suppressor. However, the mechanism of CMTM2 in HCC occurrence and development has not been well elaborated.Materials and Methods: The expression of CMTM2 was knocked-down by RNA interruption in Huh-7 and SMMC7721 cells. Cell proliferation ability was detected by CCK8 test and colony formation assay. The cell invasion and migration were measured by wound healing and Transwell assay.Results: We found that the cell proliferation was significantly increased by interruption of CMTM2 expression, both in Huh-7 and SMMC7721 cells. Moreover, down-regulated CMTM2 could promote the invasion and migration ability of HCC cells through inducing the epithelial-mesenchymal transition (EMT) process. We further discovered that both the expression of CMTM2 and the EMT-associated marker E-cadherin were decreased in the same thirty cases of HCC tissues compared with the corresponding adjacent non-tumor tissues. Pearson correlation test showed that there was a significantly positive correlation between CMTM2 and E-cadherin in HCC tissues (P< 0.05).Conclusion: Based on the results of cell model and HCC tissues, our study suggests that down-regulated CMTM2 promotes HCC metastasis through inducing the EMT process.Keywords: CMTM2, CMTM family members, HCC, metastasis, EMT

Published
2020

2. Clinical Significance of POM121 Expression in Lung Cancer.

Author

Zhang, Shidong, Zheng, Chuanjun, Li, Di, Bei, Chunhua, Zhang, Huixia, Tian, Run, Song, Xin, Zhu, Xiaonian, and Tan, Shengkui

Subjects
*LOG-rank test, *LUNG cancer, *LOGISTIC regression analysis, *LYMPHATIC metastasis, *PROTEIN expression, *BIOMARKERS
Abstract

Aims: The aim of this study was to examine the RNA and protein expression levels and clinical significance of the pore membrane protein 121 kDa (POM121) in lung cancer. Materials and Methods: Paired lung cancer and adjacent nontumor tissues were obtained from lung cancer patients to measure the expression of POM121 by quantitative reverse transcription–polymerase chain reaction and immunohistochemistry. Patient clinical and pathological data were collected to analyze their relationships with POM121 protein expression levels by chi-square test and log-rank test, respectively. Results:POM121 mRNA and protein expression were both upregulated in lung cancer tissues. POM121 protein expression was observed in 48.00% (36/75) of lung cancer tissues and 25.33% (19/75) of adjacent nontumor tissues. A chi-square analysis indicated that this difference was statistically significant (p < 0.05). Furthermore, we found that POM121 protein expression was correlated with gender, tumor node metastasis stage, and lymphatic metastasis (p < 0.05). In addition, we found a significant relationship among POM121 expression, gender, and metastasis based on a multivariate logistic regression analysis. A Kaplan–Meier survival analysis indicated that lung cancer patients with POM121 expression had a poorer prognosis than those without POM121 expression (p < 0.05). Conclusion: POM121 protein expression is associated with lung cancer metastasis and is a potential prognostic biomarker for lung cancer patients. [ABSTRACT FROM AUTHOR]

Published
2020
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3. M6A Demethylase FTO Plays a Tumor Suppressor Role in Thyroid Cancer.

Author

Tian, Run, Zhang, Shidong, Sun, Daxin, Bei, Chunhua, Li, Di, Zheng, Chuanjun, Song, Xin, Chen, Mengshi, Tan, Shengkui, Zhu, Xiaonian, and Zhang, Huixia

Subjects
THYROID cancer, DNA copy number variations, LYMPHATIC metastasis, DEMETHYLASE, SURVIVAL analysis (Biometry)
Abstract

The purpose of this study was to investigate the expression and clinical significance of N6-methyladenosine demethylase FTO in thyroid cancer. Bioinformatic analysis showed that FTO expression was downregulated in thyroid cancer tissues and correlated with lymph node metastasis in thyroid cancer patients. We conducted experimental verification by collecting Asian samples. The results of quantitative reverse transcription-PCR showed that the mRNA expression of FTO in the blood of 30 thyroid cancer patients was lower than that of the control population. At the same time, we found that FTO expression was negative in tissues of 16/56 (28.57%) thyroid cancer cases and 4/40 (10.00%) nontumor thyroid cases through the immunohistochemical method, indicating a lower FTO expression in thyroid cancer tissues than nontumor thyroid tissues (p < 0.05). In addition, the protein expression of FTO was significantly related to the tumor grade and lymph node metastasis in thyroid cancer patients (p < 0.05), but not to other clinicopathological features. Multivariate logistic regression analysis showed that FTO expression was an independent risk factor for tumor grade. Survival analysis showed no significant difference in the disease-free survival time of thyroid cancer patients between high expression and low expression groups of FTO. Furthermore, bioinformatic analysis found that promoter DNA methylation and copy number variation might cause downregulated FTO and then affect TP53 pathways in thyroid cancer. We found that FTO expression was downregulated in thyroid cancer tissues and related to the progression of thyroid cancer, suggesting a tumor suppressor role of FTO in thyroid cancer. [ABSTRACT FROM AUTHOR]

Published
2020
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