Publications by authors named "Xiangsen Ye"

6 Publications

  • Page 1 of 1

Incidence, clinical risk and prognostic factors for liver metastasis in patients with cervical cancer: a population-based retrospective study.

BMC Cancer 2021 Apr 16;21(1):421. Epub 2021 Apr 16.

Department of Clinical Laboratory, Renmin Hospital of Wuhan University, Jiefang Road 238, Wuhan, 430060, China.

Background: Cervical cancer is one of the most frequent malignancies in women, particularly metastasis resulting in a poor prognosis. However, the clinical characteristics of cervical cancer patients with advanced liver metastasis have not been well investigated. We aimed to evaluate the incidence, clinical risk and prognostic factors for hepatic metastasis in cervical cancer patients.

Materials And Methods: The clinical features of patients diagnosed with cervical cancer were collected from the Surveillance, Epidemiology and End Result (SEER) public cancer database between 2010 and 2015. Multivariate logistic and Cox regression models were performed to identify potential risk and prognostic factors for liver metastasis in patients with cervical cancer.

Results: A total of 431 patients (2.32%) developed liver metastasis in our analysis. The following characteristics were significantly associated with the development of liver metastasis: black ethnicity, uninsured status, higher tumor stage, poorer differentiated grade, non-squamous histology, non-surgery of primary site, patients with any additional lung, bone, and brain metastasis. Multivariate Cox regression showed that patients with additional lung metastasis, without radiotherapy, and without chemotherapy were negatively correlated with overall survival. Concurrent chemotherapy and radiotherapy was a favorable prognostic factor to improve overall survival, and chemotherapy showed to increase cause-specific survival. Additional lung metastasis was an independent characteristic for both risk and prognostic factors for hepatic metastasis in patients with cervical cancer.

Conclusion: Our results found several potential clinical features that may be used to assess the risk and prognosis of liver metastasis in patients with cervical cancer. These associated factors may provide clinical indications for the early identification and treatment of cervical cancer patients with hepatic metastasis.
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http://dx.doi.org/10.1186/s12885-021-08127-6DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8052699PMC
April 2021

PGRN TAMs-derived exosomes inhibit breast cancer cell invasion and migration and its mechanism exploration.

Life Sci 2021 Jan 9;264:118687. Epub 2020 Nov 9.

Key Laboratory of Clinical Laboratory Diagnostics (Ministry of Education), College of Laboratory Medicine, Chongqing Medical University, Chongqing 400016, PR China. Electronic address:

Breast cancer is one of the most malignant diseases world-wide and ranks the first among female cancers. Progranulin (PGRN) plays a carcinogenic role in breast cancer, but its mechanisms are not clear. In addition, there are few reports on the relationship between PGRN and tumor-associated macrophages (TAMs).

Aims: To investigate the effects of exosomes derived from PGRN TAMs on invasion and migration of breast cancer cells.

Main Methods: Mouse breast cancer xenograft model was constructed to explore the effect of PGRN tumor environment (TME) on breast cancer. Flow cytometry was used to compare TAMs of wild type (WT) and PGRN tumor tissue. Transwell assay, wound healing assay and western blot were used to explore the effect of WT and PGRN TAMs and their exosomes on invasion, migration and epithelial-mesenchymal transition (EMT) of breast cancer cells. MicroRNA (miRNA) assay was used to find out the differentially expressed miRNA of negative control (NC) and siPGRN-TAMs exosomes. Quantitative PCR and luciferase report assay were used to explore the target gene.

Key Findings: The lung metastasis of breast cancer of PGRN mice was inhibited. PGRN TAMs inhibited invasion, migration and EMT of breast cancer cells through their exosomes. MiR-5100 of PGRN TAMs-derived exosomes was up-regulated, which might regulate expression of CXCL12, thereby inhibiting the CXCL12/CXCR4 axis, and ultimately inhibiting the invasion, migration and EMT of breast cancer cells.

Significance: Our study elucidates a new molecular mechanism of lung metastasis of breast cancer, so it may contribute to efficient prevention and therapeutic strategies.
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http://dx.doi.org/10.1016/j.lfs.2020.118687DOI Listing
January 2021

The miR-186-3p/EREG axis orchestrates tamoxifen resistance and aerobic glycolysis in breast cancer cells.

Oncogene 2019 07 9;38(28):5551-5565. Epub 2019 Apr 9.

Key Laboratory of Diagnostic Medicine Designated by the Ministry of Education, Chongqing Medical University, 400016, Chongqing, China.

Tamoxifen resistance is one of the major challenges for its medical uses in estrogen receptor (ER)-positive breast cancer. Aerobic glycolysis, an anomalous characteristic of glucose metabolism in cancer cells, has been shown to associate with the resistance to chemotherapeutic agents. It remains, however, largely unclear whether and how tamoxifen resistance contributes to aerobic glycolysis in breast cancer. Here, we report that tamoxifen resistance is associated with enhanced glycolysis in ER-positive breast cancer cells. We demonstrate that EREG, an agonist of EGFR, has an important role in enhancing glycolysis via activating EGFR signaling and its downstream glycolytic genes in tamoxifen-resistant breast cancer cells. We further show that EREG is a direct target of miR-186-3p and that downregulation of miR-186-3p by tamoxifen results in EREG upregulation in tamoxifen-resistant breast cancer cells. Importantly, systemic delivery of cholesterol-modified agomiR-186-3p to mice bearing tamoxifen-resistant breast tumors effectively attenuates both tumor growth and [F]-fluoro-deoxyglucose ([F]-FDG) uptake. Together, our results reveal a novel molecular mechanism of resistance to hormone therapies in which the miR-186-3p/EREG axis orchestrates tamoxifen resistance and aerobic glycolysis in ER-positive breast cancer, suggesting targeting miR-186-3p as a promising strategy for therapeutic intervention in endocrine-resistant breast tumors.
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http://dx.doi.org/10.1038/s41388-019-0817-3DOI Listing
July 2019

[Verteporfin inhibits proliferation, invasion and migration of MDA-MB-231 human breast cancer cells by down-regulating the expression of Yes-associated protein].

Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi 2017 Sep;33(9):1223-1227

Ministry of Education Key Laboratory of Laboratory Medical Diagnostics, Chongqing Medical University, Chongqing 400016, China. *Corresponding author, E-mail:

Objective To investigate the effects of verteporfin on the proliferation, invasion and migration of human breast cancer MDA-MB-231 cells and the underlying mechanism. Methods MDA-MB-231 cells in the logarithmic growth phase were randomly divided into control group and verteporfin treatment group. After MDA-MB-231 cells were treated with (0, 4, 8, 12, 16) μmol/mL verteporfin, the minimal inhibitory concentration was determined by CCK-8 assay. After treatment with 4 μmol/mL verteporfin, the invasion and migration abilities of MDA-MB-231 cells were detected by Transwell invasion assay and scratch wound healing assay, respectively. The expression levels of proliferation-associated proteins c-MYC, cyclin D1, Yes-associated protein (YAP), cysteine-rich protein 61 (CYR61) and connective tissue growth factor (CTGF) in MDA-MB-231 cells treated by (0, 4, 8, 12, 16) μmol/mL verteporfin were determined by Western blotting. Results Verteporfin markedly inhibited the proliferation of MDA-MB-231 cells in a dose-dependent manner, and the minimal inhibitory concentration was 4 μmol/mL. The 4 μmol/mL verteporfin significantly inhibited the invasion and migration abilities of MDA-MB-231 cells. Verteporfin inhibited significantly the expressions of c-MYC, cyclin D1, YAP, CYR61 and CTGF. Conclusion Verteporfin significantly inhibits the proliferation, invasion and migration of MDA-MB-231 cells by down-regulating the expressions of YAP and its target genes CYR61 and CTGF.
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September 2017

Cisplatin-induced autophagy protects breast cancer cells from apoptosis by regulating yes-associated protein.

Oncol Rep 2017 Dec 16;38(6):3668-3676. Epub 2017 Oct 16.

Key Laboratory of Diagnostic Medicine Designated by the Ministry of Education, Chongqing Medical University, Yuzhong, Chongqing 400016, P.R. China.

Breast cancer is a common cause of cancer‑related deaths in women. Treatment with cisplatin exhibits some therapeutic efficacy. However, treatment optimization is required, and the mechanisms underlying the cisplatin's proapoptotic effects remain unclear. In the present study, we demonstrated that cisplatin induced apoptosis and autophagy in breast cancer cells. Autophagy induced by cisplatin played a protective role in breast cancer cells, which impaired its proapoptotic effect. Mechanistically, for the first time, we found that cisplatin treatment activated the MAPK signaling pathway and promoted autophagy via the ERK signaling pathway. Notably, we found that nuclear translocation of yes-associated protein (YAP) was regulated by cisplatin-induced autophagy, and we identified YAP as a survival input that promoted survival in cisplatin-treated breast cancer cells. These findings revealed that administration of cisplatin along with an autophagy inhibitor is a promising therapeutic strategy for treating breast cancer.
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http://dx.doi.org/10.3892/or.2017.6035DOI Listing
December 2017

Invalidation of mitophagy by FBP1-mediated repression promotes apoptosis in breast cancer.

Tumour Biol 2017 Jun;39(6):1010428317708779

Key Laboratory of Diagnostic Medicine Designated by the Ministry of Education, Chongqing Medical University, Chongqing, P.R. China.

Fructose-1,6-bisphosphatase 1, a rate-limiting enzyme in gluconeogenesis, was recently shown to be a tumor suppressor. However, the functions of fructose-1,6-bisphosphatase 1 in the regulation of mitophagy and apoptosis remain unknown. Here, we investigated the effects of fructose-1,6-bisphosphatase 1 on mitophagy and apoptosis as well as their underlying mechanisms in breast cancer cells. In this work, the messenger RNA and protein expression of various molecules were determined by quantitative realtime polymerase chain reaction and western blot, respectively. Gene-expression correlations were obtained from The Cancer Genome Atlas Breast Cancer database and analyzed using cBioPortal. The levels of cellular reactive oxygen species and apoptotic index were detected by flow cytometry. The mitochondrial membrane potentials were assessed with a JC-1 fluorescent sensor. Subcellular structures were observed under a transmission electron microscope. The intracellular distribution of translocase of outer membrane 20 was detected by immunofluorescence staining. Protein-protein interactions were analyzed by immunoprecipitation. Our results indicated that fructose-1,6-bisphosphatase 1 expression was negatively correlated with autophagy level in breast cancer. Fructose-1,6-bisphosphatase 1 restrained autophagy activity by increasing the level of p62 and decreasing the levels of LC3 and Beclin 1. Additionally, fructose-1,6-bisphosphatase 1 promoted cell apoptosis by upregulating the levels of intracellular ROS and expression of pro-apoptotic proteins such as cleaved PARP, cleaved Caspase 3, and Bax and downregulating the levels of anti-apoptotic proteins such as PARP, Caspase 3, and Bcl-2. Finally, fructose-1,6-bisphosphatase 1 limited the efficient removal of diseased mitochondria and reduced the messenger RNA and protein expressions of HIF-1α, BNIP3L/NIX, and BNIP3. More importantly, fructose-1,6-bisphosphatase 1 facilitated co-action between Bcl-2 and Beclin 1, which may be important in the mechanism of fructose-1,6-bisphosphatase 1-mediated mitophagy inhibition. In summary, loss of mitophagy by fructose-1,6-bisphosphatase 1-mediated repression promotes apoptosis in breast cancer.
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http://dx.doi.org/10.1177/1010428317708779DOI Listing
June 2017
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