Jiang Geng

Dr. Jiang Geng


Research Focus & Metrics

Academic Career Length

18Years (2009-Present)

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

Representative Publications

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18 April 2019 in Journal of Experimental & Clinical Cancer Research
Verified
Journal Article
Open access
PDF file
WMWeipu Mao
Weipu Mao
XHXin Huang
Xin Huang
LWLongsheng Wang
Longsheng Wang
ZZZiwei Zhang
Ziwei Zhang
MLMengnan Liu
Mengnan Liu
JGJiang Geng
Jiang Geng
Background: FGFR3 plays an important role in the development of bladder cancer (BCa). Hsa_circ_0068871 is a circRNA generated from several exons of FGFR3. However, the potential functional role of hsa_circ_0068871 in BCa remains largely unknown. Here we aim to evaluate the role of hsa_circ_0068871 in BCa. Methods: We selected miR-181a-5p as the potential target miRNA of hsa_circ_0068871. The expression levels of hsa_circ_0068871 and miR-181a-5p were examined in BCa tissues and paired adjacent normal tissues by quantitative real-time PCR. To characterize the function of hsa_circ_0068871, BCa cell lines were stably infected with lentivirus targeting hsa_circ_0068871, followed by examinations of cell proliferation, migration and apoptosis. In addition, xenografts experiment in nude mice were performed to evaluate the effect of hsa_circ_0068871 in BCa. Biotinylated RNA probe pull-down assay, fluorescence in situ hybridization and luciferase reporter assay were conducted to confirm the relationship between hsa_circ_0068871, miR-181a-5p and FGFR3. Results: Hsa_circ_0068871 is over-expressed in BCa tissues and cell lines, whereas miR-181a-5p expression is repressed. Depletion of has_circ_0068871 or upregulation of miR-181a-5p inhibited the proliferation and migration of BCa cells in vitro and in vivo. Mechanistically, hsa_circ_0068871 upregulated FGFR3 expression and activated STAT3 by targeting miR-181a-5p to promote BCa progression. Conclusions: Hsa_circ_0068871 regulates the miR-181a-5p/FGFR3 axis and activates STAT3 to promote BCa progression, and it may serve as a potential biomarker.

1 April 2014 in International Urology and Nephrology
Verified
Journal Article
Closed access
PDF file
THTian-Bao Huang
Tian-Bao Huang
YYYang Yan
Yang Yan
ZGZhui-Feng Guo
Zhui-Feng Guo
XZXiao-Long Zhang
Xiao-Long Zhang
HLHuan Liu
Huan Liu
JZJun-Hua Zheng
Jun-Hua Zheng

1 January 2019 in Journal of Cancer
Verified
Journal Article
Open access
WMWeipu Mao
Weipu Mao
ZZZiwei Zhang
Ziwei Zhang
XHXin Huang
Xin Huang
JFJie Fan
Jie Fan
JGJiang Geng
Jiang Geng
Purpose: We aimed to reveal the effects of marital status on survival outcomes in patients with penile cancer.

1 August 2019 in Translational Oncology
Verified
Journal Article
Open access
WMWeipu Mao
Weipu Mao
MLMing Luo
Ming Luo
XHXin Huang
Xin Huang
QWQian Wang
Qian Wang
JFJie Fan
Jie Fan
JGJiang Geng
Jiang Geng
Lumican (LUM) is differentially expressed between normal and cancer tissues. The purpose of this study was to investigate the role of LUM in the proliferation and migration of bladder cancer (BCa) cells. Our study included 97 cases of BCa diagnosis from our hospital between June 2013 and June 2016. The expression of LUM was analyzed by immunohistochemistry and Western blot. To characterize the function of LUM, BCa cells were stably infected with a lentivirus against LUM, and cell proliferation, migration and cell cycle were investigated. In addition, xenograft experiments were performed in nude mice to evaluate the role of LUM in BCa. Our results showed that LUM was overexpressed in BCa tissues and cell lines in comparison to normal tissues. LUM expression was related to pathological type, T stage and N stage (P < .05). In addition, depletion of LUM inhibited the proliferation and migration of BCa cells by inactivating MAPK signaling. In conclusion, LUM promotes the proliferation and migration of BCa cells and may serve as a potential therapeutic target for BCa.

22 October 2021 in Frontiers in Cell and Developmental Biology
Verified
Journal Article
Open access
WMWeipu Mao
Weipu Mao
KWKeyi Wang
Keyi Wang
SSSi Sun
Si Sun
JWJianping Wu
Jianping Wu
MCMing Chen
Ming Chen
MLMing Luo
Ming Luo
Background: Inhibitors of DNA-binding (ID) proteins are important regulators of cell proliferation and differentiation. The aim of this study was to evaluated the role of ID proteins in bladder cancer (BCa) and related molecular mechanisms.Methods: The TCGA database was analyzed for the expression and clinical significance of ID proteins. The expression of ID2 was determined by qRT-PCR, immunohistochemical staining and western blot. The role of ID2 was determined by CCK-8, colony formation, wound healing, transwell and xenograft tumor assays, and the potential mechanism of ID2 in BCa was investigated by RNA sequencing.Results: ID2 expression was significantly downregulated in TCGA database and clinical samples, and high ID2 expression was associated with low-grade tumor staging and correlated with better overall survival, disease specific survival (DSS) and progress free interval (PFI). In vivo and in vitro experiments showed that knockdown of ID2 promoted proliferation, migration, invasion and metastasis of BCa cells, while overexpression of ID2 significantly inhibited cell proliferation, migration, invasion and metastasis. Mechanistically, ID2 acts as a tumor suppressor through PI3K/AKT signaling pathway to inhibit the progression and metastasis of BCa.Conclusion: Our results suggest that ID2 exerts tumor suppressive effects in BCa through PI3K/AKT signaling pathway, and altered ID2 expression can be used as a biomarker of BCa progression and metastasis.

4 December 2019 in Kidney and Blood Pressure Research
Verified
Journal Article
Open access
PDF file
WMWeipu Mao
Weipu Mao
SLShenghua Liu
Shenghua Liu
KWKeyi Wang
Keyi Wang
MWMiao Wang
Miao Wang
HSHeng Shi
Heng Shi
JGJiang Geng
Jiang Geng
Background: Serum cystatin C (CysC) is still becoming used as a marker of renal function but is far from being commonly used worldwide. The purpose of this study was to characterize the ureteral calculi patients with hydronephrosis-caused CysC changes in renal function. Methods: To better reflect the changes of renal function, we constructed models of ureteral obstruction in rats to mimic the hydronephrosis caused by human ureteral calculi. Moreover, our study included 200 patients diagnosed with ureteral calculi in our hospital between June 2017 and 2018. We compared the estimated glomerular filtration rate using different equations based on CysC and/or serum creatinine (SCr). Results: We found that the expression of CysC and SCr increased with the prolonged obstruction time by enzyme linked immunosorbent assay. Moreover, quantitative real-time polymerase chain reaction, Western blot and immunohistochemistry further demonstrated that the expression of CysC increases with the degree of hydronephrosis. Among 200 patients with ureteral calculi, 40 (20.0%) had no hydronephrosis, 110 (55.0%) had mild hydronephrosis, 32 (16.0%) had moderate hydronephrosis and 18 (9.0%) had severe hydronephrosis. As the degree of hydronephrosis increased, the expression of neutrophil percentage, CysC, blood urea nitrogen, SCr and serum uric acid also increased. Multivariate analyses demonstrated that only CysC was an independent risk factor for hydronephrosis (p = 0.003). In addition, CysC and the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) CysC equation showed the highest veracity in renal function estimation of patients with hydronephrosis caused by ureteral calculus. Conclusion: For patients with hydronephrosis caused by ureteral calculi, CysC better reflects the changes in renal function, and the CKD-EPI CysC equation has the highest accuracy.