Fei Kuang

Dr. Fei Kuang

Department of Thyroid & Hernia Surgery, Chinese People's Liberation Army, Beijing, China
orcid

Research Focus & Metrics

Academic Career Length

20Years (2007-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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4 January 2018 in Cell & Bioscience
Verified
Journal Article
Open access
PDF file
JYJun Ying
Jun Ying
HZHaiyang Zhou
Haiyang Zhou
PLPeng Liu
Peng Liu
QYQing You
Qing You
FKFei Kuang
Fei Kuang
ZHZhi-Qian Hu
Zhi-Qian Hu
The metastasis of colorectal cancer frequently tends to liver, which is one of the three leading causes of cancer-related deaths worldwide. Growing evidence showed that aspirin could effectively inhibit liver metastasis of colorectal cancer. However, the potential mechanism has not been fully understood. Mouse splenic vein metastasis assay was used to examine the metastatic ability of colon cancer cells in vivo. And wound healing and transwell assay were applied to detect the metastasis potential of C26 and HCT116 colon cancer cell lines in vitro. RT-PCR and western blotting were used to explore Toll-like receptor 4 (TLR4) expression in colon cancer cell lines. The functions of TLR4 in the migration of the colon cancer cell line were analyzed by infecting cells with lentivirus containing TLR4 siRNA. We demonstrated that lipopolysaccharides (LPS) could enhance the metastasis potential of C26 and HCT116 colon cancer cell lines. However, aspirin effectively decreased the metastasis capacity of colon cancer cells in vitro and in vivo. We found that the enhancement of LPS on the migration of colon cancer cells by inducing epithelial-mesenchymal transition (EMT) phenotype demonstrated a TLR4-dependent manner. Aspirin treatment lead to the downregulation of TLR4 on C26 cells which resulted in the decrease of C26 cells migration and EMT phenotype that induced by LPS. Additionally, the inhibitory effect from aspirin on the expression of TLR4 on C26 cells leads to the downregulation of NF-κB. The results of our study indicate that LPS origin from intestinal flora may promote the metastasis of colon cancer to liver and aspirin may inhibit the metastasis of colon cancer by inhibiting the expression of TLR4.

10 June 2022 in Frontiers in Oncology
Verified
Journal Article
Open access
DLDe Luo
De Luo
FKFei Kuang
Fei Kuang
JDJuan Du
Juan Du
MZMengjia Zhou
Mengjia Zhou
XLXiangdong Liu
Xiangdong Liu
SSSong Su
Song Su
Objective: The aim of this study was to assess the diagnostic ability of artificial intelligence (AI) in the detection of early upper gastrointestinal cancer (EUGIC) using endoscopic images. Methods: Databases were searched for studies on AI-assisted diagnosis of EUGIC using endoscopic images. The pooled area under the curve (AUC), sensitivity, specificity, positive likelihood ratio (PLR), negative likelihood ratio (NLR), and diagnostic odds ratio (DOR) with 95% confidence interval (CI) were calculated. Results: Overall, 34 studies were included in our final analysis. Among the 17 image-based studies investigating early esophageal cancer (EEC) detection, the pooled AUC, sensitivity, specificity, PLR, NLR, and DOR were 0.98, 0.95 (95% CI, 0.95–0.96), 0.95 (95% CI, 0.94–0.95), 10.76 (95% CI, 7.33–15.79), 0.07 (95% CI, 0.04–0.11), and 173.93 (95% CI, 81.79–369.83), respectively. Among the seven patient-based studies investigating EEC detection, the pooled AUC, sensitivity, specificity, PLR, NLR, and DOR were 0.98, 0.94 (95% CI, 0.91–0.96), 0.90 (95% CI, 0.88–0.92), 6.14 (95% CI, 2.06–18.30), 0.07 (95% CI, 0.04–0.11), and 69.13 (95% CI, 14.73–324.45), respectively. Among the 15 image-based studies investigating early gastric cancer (EGC) detection, the pooled AUC, sensitivity, specificity, PLR, NLR, and DOR were 0.94, 0.87 (95% CI, 0.87–0.88), 0.88 (95% CI, 0.87–0.88), 7.20 (95% CI, 4.32–12.00), 0.14 (95% CI, 0.09–0.23), and 48.77 (95% CI, 24.98–95.19), respectively. Conclusions: On the basis of our meta-analysis, AI exhibited high accuracy in diagnosis of EUGIC. Systematic Review Registration: https://www.crd.york.ac.uk/PROSPERO/, identifier PROSPERO (CRD42021270443).

31 March 2023 in International Journal of Surgery
Verified
Journal Article
Open access
DLDe Luo
De Luo
XCXin-Pei Chen
Xin-Pei Chen
YDYang Dai
Yang Dai
FKFei Kuang
Fei Kuang
MKMao-Ji Kang
Mao-Ji Kang
SSSong Su
Song Su
Background: There is still a lack of knowledge on the association between cholecystectomy and liver disease. This systematic review and meta-analysis was conducted to summarize the available evidence on the association of cholecystectomy with liver disease and quantify the magnitude of the risk of liver disease after cholecystectomy. Methods: PubMed, Embase, Web of Science, and Cochrane Library were searched systematically from database inception to January 2023 to identify eligible studies that evaluated the association between cholecystectomy and the risk of liver disease. Meta-analysis was conducted to obtain a summary odds ratio (OR) and 95% confidence interval (CI) using a random-effects model. Results: We identified 20 studies with a total of 27,320,709 individuals and 283,633 liver disease cases. Cholecystectomy was associated with an increased risk of liver disease (OR 1.63, 95% CI 1.34-1.98). In particular, cholecystectomy was found to be significantly associated with a 54% increased risk of nonalcoholic fatty liver disease (OR 1.54, 95% CI 1.18-2.01), a 173% increased risk of cirrhosis (OR 2.73, 95% CI 1.81-4.12), and a 46% increased risk of primary liver cancer (OR 1.46, 95% CI 1.18-1.82). Conclusions: There is an association between cholecystectomy and the risk of liver disease. Our results suggest that strict surgical indications should be implemented to reduce unnecessary cholecystectomy. Additionally, the routine assessment of liver disease is necessary for patients with a history of cholecystectomy. More prospective large-sample studies are required for better estimates of the risk. Export

14 September 2022 in Liver International
Verified
Journal Article
Closed access
DLDe Luo
De Luo
XCXinpei Chen
Xinpei Chen
JDJuan Du
Juan Du
BMBingjie Mei
Bingjie Mei
AWAnkang Wang
Ankang Wang
SSSu Song
Su Song

1 February 2019 in Pathology - Research and Practice
Verified
Journal Article
Closed access
YLYuee Liu
Yuee Liu
WHWei Huang
Wei Huang
XGXianhua Gao
Xianhua Gao
FKFei Kuang
Fei Kuang

4 March 2012 in Molecular Medicine Reports
Verified
Journal Article
Open access
PDF file
QZQing-Mei Zhao
Qing-Mei Zhao
FKFei Kuang
Fei Kuang
HWHan Wu
Han Wu
YZYu-Hao Zhang
Yu-Hao Zhang
Colorectal cancer is one of the most commonly diagnosed types of cancer and is a leading cause of cancer-associated mortality worldwide. Short chain enoyl coenzyme A hydratase 1 (ECHS1) is an important gene involved in the mitochondrial fatty acid β-oxidation pathway. In addition, ECHS1 has been implicated in a variety of cancers, including breast, prostate, colon and liver cancer. The aim of the present study was to examine the expression of ECHS1 in the human HCT-8 colorectal cancer cell line. The results showed that ECHS1 expression was significantly increased in poorly-differentiated cells compared with that in well-differentiated cells. In order to further investigate the functions of ECHS1 in colorectal cancer cells, a stably transfected HCT-8 cell line expressing small interfering (si)RNA targeting the ECHS1 gene was established. The expression of the ECHS1 siRNA was found to reduce ECHS1 protein levels in ECHS1-silenced cells by >40%. Cell proliferation and cell migration of the siECHS1 cells were characterized using Cell Counting Kit-8 and Transwell assays, respectively, the results of which showed that the constitutive knockdown of the ECSH1 gene in HCT-8 cells significantly inhibited cell proliferation and migration. Furthermore, decreased levels of Akt and glycogen synthase kinase (GSK)3β phosphorylation were observed in ECHS1-silenced HCT-8 cells compared with that of parental or pU6 empty vector-transfected cells. In conclusion, the results of the present study suggested that ECHS1 may have an important role in colorectal cancer cell proliferation and migration via activation of Akt- and GSK3β-associated signaling pathways.