• Complex
  • Title
  • Author
  • Keyword
  • Abstract
  • Scholars
Search
High Impact Results & Cited Count Trend for Year Keyword Cloud and Partner Relationship

Query:

学者姓名:李磊

Refining:

Co-Author

Submit Unfold

Language

Submit

Clean All

Export Sort by:
Default
  • Default
  • Title
  • Year
  • WOS Cited Count
  • Impact factor
  • Ascending
  • Descending
< Page ,Total 3 >
PrLZ increases prostate cancer docetaxel resistance by inhibiting LKB1/AMPK-mediated autophagy SCIE PubMed Scopus
期刊论文 | 2018 , 8 (1) , 109-123 | THERANOSTICS
WoS CC Cited Count: 4 SCOPUS Cited Count: 4
Abstract&Keyword Cite

Abstract :

Rationale: Docetaxel-mediated chemotherapy is the first-line standard approach and has been determined to show a survival advantage for metastatic castration-resistant prostate cancer (mCRPC) patients. However, a substantial proportion of patients eventually becomes refractory due to drug resistance. The detailed mechanisms remain unclear. We have previously reported that Prostate Leucine Zipper (PrLZ), a specific oncogene of prostate cancer (PCa), promotes PCa cell growth at the castration-resistant stage, thus suggesting a vital role of PrLZ in the progression of CRPC. In this study, we aimed to investigate the role of PrLZ in docetaxel resistance in PCa, focusing on PrLZ-regulating autophagy pathway. Methods: Human PCa PC3, LNCaP and C4-2 cell lines were used as the model system in vitro and PCa xenografts and PrLZ-knockout mice were used as the model system in vivo. Docetaxel-induced cell death and apoptosis in PCa were determined by MTT and flow cytometry assay. The role of PrLZ on the regulation of autophagy and liver kinase B1/AMP-activated protein kinase (LKB1/AMPK) signaling pathway was analyzed using immunoblotting, immunoprecipitation, siRNA silencing and plasmid overexpression. Results: PrLZ increased docetaxel-mediated drug resistance both in vitro and in vivo. Mechanistic dissection revealed that PrLZ interacted with LKB1 and further inhibited the activation of LKB1/AMPK signals, which negatively contributed to the induction of autophagy. Moreover, PrLZ/LKB1-mediated autophagy conferred resistance to docetaxel-induced cell death and apoptosis both in vitro and in vivo. Conclusion: These findings identify a novel role of PrLZ in autophagy manipulation and provide new insight into docetaxel chemoresistance in PCa, suggesting a new strategy for treating mCRPC by targeting this newly identified signaling pathway.

Keyword :

PrLZ LKB1 Prostate cancer Docetaxel Autophagy

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 Zeng, Jin , Liu, Wei , Fan, Yi-Zeng et al. PrLZ increases prostate cancer docetaxel resistance by inhibiting LKB1/AMPK-mediated autophagy [J]. | THERANOSTICS , 2018 , 8 (1) : 109-123 .
MLA Zeng, Jin et al. "PrLZ increases prostate cancer docetaxel resistance by inhibiting LKB1/AMPK-mediated autophagy" . | THERANOSTICS 8 . 1 (2018) : 109-123 .
APA Zeng, Jin , Liu, Wei , Fan, Yi-Zeng , He, Da-Lin , Li, Lei . PrLZ increases prostate cancer docetaxel resistance by inhibiting LKB1/AMPK-mediated autophagy . | THERANOSTICS , 2018 , 8 (1) , 109-123 .
Export to NoteExpress RIS BibTex
A novel 450-nm blue laser system for surgical applications: efficacy of specific laser-tissue interactions in bladder soft tissue Scopus PubMed
期刊论文 | 2018 | Lasers in Medical Science
Abstract&Keyword Cite

Abstract :

© 2018, Springer-Verlag London Ltd., part of Springer Nature. Low-power blue laser allows clean cutting with little bleeding and no undesired coagulations in adjacent tissues; however, studies on high-power blue laser soft tissue ablation properties, including vaporization and coagulation, have not been reported yet. The purpose of this study is to evaluate and analyze the ablation efficacy and coagulation properties of bladder epithelium tissues with a 30-W 450-nm wavelength blue laser. Well-designed ex vivo experiments compared blue laser and 532-nm LBO green laser, both with laser power up to 30 W, for porcine bladder tissue vaporization and coagulation at different experimental parameter settings. At working distance of 1 mm and sweeping speed of 1.5 mm/s, the vaporization efficiency of blue laser and green laser was 5.14mm3/s and 1.20mm3/s, while the depth of coagulation layer was 460 ± 70 μm and 470 ± 80 μm, respectively. We found both blue laser and green laser have excellent efficacy of tissue vaporization and similar tissue coagulation properties. Moreover, in a set of in vivo experiments simulated laser transurethral resection (TUR) surgery on dogs, we found both blue laser and green laser exhibited similar and satisfactory vaporization and coagulation outcomes. Taken together, our results demonstrate that a 450-nm wavelength high-power diode blue laser, like 532-nm wavelength green laser, is capable to produce high efficient tissue vaporization, low-laser tissue penetration, good tissue coagulation, and has low thermal damage to adjacent tissues. Therefore, a 30-W blue diode laser could be a new and safe alternative for surgeries of superficial bladder diseases.

Keyword :

Bladder Blue laser Coagulation Vaporization

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 Jiang, Da-Li , Yang, Zheng , Liu, Guo-Xiong et al. A novel 450-nm blue laser system for surgical applications: efficacy of specific laser-tissue interactions in bladder soft tissue [J]. | Lasers in Medical Science , 2018 .
MLA Jiang, Da-Li et al. "A novel 450-nm blue laser system for surgical applications: efficacy of specific laser-tissue interactions in bladder soft tissue" . | Lasers in Medical Science (2018) .
APA Jiang, Da-Li , Yang, Zheng , Liu, Guo-Xiong , Wu, Kaijie , Fan, Jinhai , Wu, Dapeng et al. A novel 450-nm blue laser system for surgical applications: efficacy of specific laser-tissue interactions in bladder soft tissue . | Lasers in Medical Science , 2018 .
Export to NoteExpress RIS BibTex
CD54-NOTCH1 axis controls tumor initiation and cancer stem cell functions in human prostate cancer SCIE PubMed Scopus
期刊论文 | 2017 , 7 (1) , 67-80 | THERANOSTICS | IF: 8.537
WoS CC Cited Count: 4 SCOPUS Cited Count: 4
Abstract&Keyword Cite

Abstract :

Cancer stem cells (CSCs) are considered one of the key contributors to chemoresistance and tumor recurrence. Therefore, the precise identification of reliable CSC markers and clarification of the intracellular signaling involved in CSCs remains a great challenge in fields relating to cancer biology. Here, we implemented a novel chemoresistant prostate cancer patient-derived xenograft (PDX) model in NOD/SCID mice and identified CD54 as a candidate gene among the most highly enriched gene expression profiles in prostate tumors exposed to chronic cisplatin administration. Additional in vitro and in vivo assays showed that CD54 played a critical role in the self-renewal and tumorigenesis of prostate CSCs. Moreover, silencing CD54 greatly reduced the tumorigenesis of prostate cancers both in vitro and in vivo and significantly extended the survival time of tumor-bearing mice in a prostate cancer xenograft model. Dissection of the molecular mechanism revealed that the p38-Notch1 axis was the main downstream signaling pathway in CD54-mediated regulation of CSCs in prostate cancers. Together, these results established that CD54 could be a novel reliable prostate CSC marker and provided a new potential therapeutic target in prostate cancer via CD54-Notch1 signaling.

Keyword :

prostate cancer cancer stem cells CD54 NOTCH1

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 Li, Chong , Liu, Shengwu , Yan, Ruping et al. CD54-NOTCH1 axis controls tumor initiation and cancer stem cell functions in human prostate cancer [J]. | THERANOSTICS , 2017 , 7 (1) : 67-80 .
MLA Li, Chong et al. "CD54-NOTCH1 axis controls tumor initiation and cancer stem cell functions in human prostate cancer" . | THERANOSTICS 7 . 1 (2017) : 67-80 .
APA Li, Chong , Liu, Shengwu , Yan, Ruping , Han, Ning , Wong, Kwok-Kin , Li, Lei . CD54-NOTCH1 axis controls tumor initiation and cancer stem cell functions in human prostate cancer . | THERANOSTICS , 2017 , 7 (1) , 67-80 .
Export to NoteExpress RIS BibTex
Preclinical Study using Malat1 Small Interfering RNA or Androgen Receptor Splicing Variant 7 Degradation Enhancer ASC-J9 (R) to Suppress Enzalutamide-resistant Prostate Cancer Progression SCIE PubMed Scopus
期刊论文 | 2017 , 72 (5) , 835-844 | EUROPEAN UROLOGY | IF: 17.581
WoS CC Cited Count: 11 SCOPUS Cited Count: 15
Abstract&Keyword Cite

Abstract :

Background: While androgen-deprivation-therapy with the recently developed antiandrogen enzalutamide (Enz) shows promising therapeutic benefits in men with metastatic castration-resistant prostate cancer (PCa), many patients develop resistance to Enz, which may involve the induction of the androgen receptor (AR) splicing variant 7 (AR-v7). Objective: Our aim is to identify the mechanisms responsible for AR-v7 production and to develop novel preclinical approaches to suppress the Enz-resistant (EnzR) PCa. Design, setting, and participants: We established EnzR-PCa cell lines and examined the long noncoding RNA Malat1 (Malat1) function in conferring Enz resistance. We also examined the in vivo effects of Malat1 short interfering RNA and the AR-v7 degradation enhancer, ASC-J9 (R). Outcome measurements and statistical analysis: Enz resistance and expression of Malat1 and AR-v7. All statistical comparisons were analyzed with a t-test or one way analysis of variance followed by t-test. Results and limitations: We demonstrated that Malat1 is indispensable for Enz-induced AR-v7 production in VCaP and EnzR-C4-2 cells. Weobserved increased AR-v7 and Malat1 expression in our established EnzR-PCa cell lines and in some PCa patients who received Enz treatment. Targeting the Malat1/AR-v7 axis resulted in altering the PCa resistance to androgen deprivation therapy with Enz. The limitation of this study includes the small sample size from the same human patients before and after receiving Enz treatment. Conclusions: Targeting the Malat1/AR-v7 axis via Malat1-short interfering RNA or AR-v7 degradation enhancer ASC-J9 (R) in EnzR-PCa cell lines and mouse models suppressed EnzR-PCa progression. Patient summary: Androgen deprivation therapy-enzalutamide treatment may not be the best choice for prostate cancer patients who have higher expression of the Malat1/androgen receptor splicing variant 7 axis, and new therapies using Malat1-short interfering RNA or ASC-J91 may be developed in the future to better suppress enzalutamide-resistant prostate cancer. (C) 2017 European Association of Urology. Published by Elsevier B.V. All rights reserved.

Keyword :

Malat1 Enzalutamide PCa AR-v7

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 Wang, Ronghao , Sun, Yin , Li, Lei et al. Preclinical Study using Malat1 Small Interfering RNA or Androgen Receptor Splicing Variant 7 Degradation Enhancer ASC-J9 (R) to Suppress Enzalutamide-resistant Prostate Cancer Progression [J]. | EUROPEAN UROLOGY , 2017 , 72 (5) : 835-844 .
MLA Wang, Ronghao et al. "Preclinical Study using Malat1 Small Interfering RNA or Androgen Receptor Splicing Variant 7 Degradation Enhancer ASC-J9 (R) to Suppress Enzalutamide-resistant Prostate Cancer Progression" . | EUROPEAN UROLOGY 72 . 5 (2017) : 835-844 .
APA Wang, Ronghao , Sun, Yin , Li, Lei , Niu, Yuanjie , Lin, Wanying , Lin, Changyi et al. Preclinical Study using Malat1 Small Interfering RNA or Androgen Receptor Splicing Variant 7 Degradation Enhancer ASC-J9 (R) to Suppress Enzalutamide-resistant Prostate Cancer Progression . | EUROPEAN UROLOGY , 2017 , 72 (5) , 835-844 .
Export to NoteExpress RIS BibTex
Androgen-deprivation therapy with enzalutamide enhances prostate cancer metastasis via decreasing the EPHB6 suppressor expression SCIE PubMed Scopus
期刊论文 | 2017 , 408 , 155-163 | CANCER LETTERS | IF: 6.491
WoS CC Cited Count: 2 SCOPUS Cited Count: 3
Abstract&Keyword Cite

Abstract :

Early studies suggested that using ADT with the recently developed anti-androgen Enzalutamide (Enz, also named as MDV3100 could extent castration resistant prostate cancer (CRPC) patients' survival an extra 4.8 months. Yet the therapy in most patients might eventually fail due to development of Enz-resistance. Here we found Enz might also increase some unwanted side-effects via increasing the CRPC cell invasion that might involve altering the Enz-mediated androgen receptor (AR)/EPHB6 suppressor/JNK signaling. Results from multiple clinical surveys also indicated that EPHP6 might function as a suppressor of PCa metastasis. Mechanism dissection revealed that Enz-mediated AR might function via binding to the androgen-response-element (ARE) on the EPHB6 promoter to decrease EPHB6 suppressor expression, which might then activate the phosphorylation of JNK signals to increase the CRPC cell invasion. Targeting this newly identified AR/EPHB6/JNK signaling with JNK inhibitor (SP600125) may then block/reverse the Enz-increased CRPC cell invasion. Collectively, our results suggest that Enz may increase CRPC cell invasion via altering the AR/EPHB6/JNK/MMP9 signaling and targeting this newly identified signaling may help us to increase the Enz efficacy to better suppress the CRPC at the later metastatic stage. (C) 2017 Elsevier B.V. All rights reserved.

Keyword :

Prostate cancer EPHB6 Androgen receptor

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 Chen, Jiaqi , Li, Lei , Yang, Zhao et al. Androgen-deprivation therapy with enzalutamide enhances prostate cancer metastasis via decreasing the EPHB6 suppressor expression [J]. | CANCER LETTERS , 2017 , 408 : 155-163 .
MLA Chen, Jiaqi et al. "Androgen-deprivation therapy with enzalutamide enhances prostate cancer metastasis via decreasing the EPHB6 suppressor expression" . | CANCER LETTERS 408 (2017) : 155-163 .
APA Chen, Jiaqi , Li, Lei , Yang, Zhao , Luo, Jie , Yeh, Shuyuan , Chang, Chawnshang . Androgen-deprivation therapy with enzalutamide enhances prostate cancer metastasis via decreasing the EPHB6 suppressor expression . | CANCER LETTERS , 2017 , 408 , 155-163 .
Export to NoteExpress RIS BibTex
Capsaicin enhances anti-proliferation efficacy of pirarubicin via activating TRPV1 and inhibiting PCNA nuclear translocation in 5637 cells SCIE PubMed Scopus
期刊论文 | 2016 , 13 (1) , 881-887 | MOLECULAR MEDICINE REPORTS | IF: 1.692
WoS CC Cited Count: 12 SCOPUS Cited Count: 12
Abstract&Keyword Cite

Abstract :

The recurrence of bladder cancer after surgery with or without chemotherapy remains a major challenge in bladder cancer treatment. Previous studies have shown that transient receptor potential vanilloid 1 (TRPV1) acts as a tumor suppressor through inducing apoptosis in bladder cancer cells. However, whether activation of TRPV1 has any synergistic effects with pirarubicin (THP), one of main drugs used in urinary bladder instillation chemotherapy to improve chemotherapeutic efficacy has remained elusive. The present study verified that TRPV1 was differentially expressed in bladder cancer cell lines. Furthermore, activation of TRPV1 by capsaicin was shown to induce growth inhibition of 5637 cells in which TRPV1 was highly expressed, while the growth of T24 cells, which express TRPV1 at low levels, was not affected. In addition, the present study demonstrated that activation of TRPV1 enhanced the anti-proliferative effects of pirarubicin using an MTT assay and cell cycle analysis. Finally, immunofluorescent microscopy revealed that activation of TRPV1 prevented the translocation of proliferating cell nuclear antigen to the nucleus. This phenomenon was reversed by pre-treatment with capsazepine, a specific TRPV1 antagonist. In conclusion, the present study confirmed the anti-tumor activity of TRPV1 against bladder cancer. Activation of TRPV1 may be applied as a novel strategy to treat bladder cancer or enhance the therapeutic efficacy of traditional chemotherapeutic drugs.

Keyword :

transient receptor potential vanilloid 1 proliferating cell nuclear antigen capsaicin chemotherapy pirarubicin

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 Zheng, Long , Chen, Jiaqi , Ma, Zhenkun et al. Capsaicin enhances anti-proliferation efficacy of pirarubicin via activating TRPV1 and inhibiting PCNA nuclear translocation in 5637 cells [J]. | MOLECULAR MEDICINE REPORTS , 2016 , 13 (1) : 881-887 .
MLA Zheng, Long et al. "Capsaicin enhances anti-proliferation efficacy of pirarubicin via activating TRPV1 and inhibiting PCNA nuclear translocation in 5637 cells" . | MOLECULAR MEDICINE REPORTS 13 . 1 (2016) : 881-887 .
APA Zheng, Long , Chen, Jiaqi , Ma, Zhenkun , Liu, Wei , Yang, Fei , Yang, Zhao et al. Capsaicin enhances anti-proliferation efficacy of pirarubicin via activating TRPV1 and inhibiting PCNA nuclear translocation in 5637 cells . | MOLECULAR MEDICINE REPORTS , 2016 , 13 (1) , 881-887 .
Export to NoteExpress RIS BibTex
FGF2-mediated reciprocal tumor cell-endothelial cell interplay contributes to the growth of chemoresistant cells: a potential mechanism for superficial bladder cancer recurrence SCIE PubMed Scopus
期刊论文 | 2016 , 37 (4) , 4313-4321 | TUMOR BIOLOGY | IF: 3.65
WoS CC Cited Count: 3 SCOPUS Cited Count: 3
Abstract&Keyword Cite

Abstract :

Patients with superficial bladder cancer can be definitively cured by one single transurethral resection (TUR) with additional intravesical chemotherapy; however, up to 75 % of cases display frequent and multiple recurrences. One of the major causes of recurrence is that chemotherapeutic drugs used in intravesical regimens may induce chemoresistance. However, the mechanisms by which these chemoresistant cells develop into recurrent tumors remain unclear. Recent clinical evidence revealed that the expression of pro-angiogenic factor FGF2 was associated with early local relapse in patients with superficial bladder cancer. In this study, we conducted a preliminary investigation of the mechanisms of chemoresistant cells mediated bladder cancer recurrence, focusing on FGF2-initiated tumor cell-endothelial cell interaction on chemoresistant cancer cell growth. We found that the expression of FGF2 was increased in chemoresistant bladder cell lines and in bladder tissues after intravesical chemotherapy. Although chemoresistant bladder cells grow slower than parental cells, chemoresistant bladder cancer cells had stronger ability than parental cells to stimulate endothelial cell migration, growth, and tube formation by producing FGF2. Inversely, endothelial cells significantly promoted chemoresistant bladder cancer growth in vitro and in vivo. Thus, targeting chemotherapy-induced FGF2 upregulation may provide a promising approach to manage the recurrence of superficial bladder cancer.

Keyword :

Bladder cancer Recurrence Chemoresistance Endothelial cell FGF2

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 Chen, Yule , Zhu, Guodong , Wu, Kaijie et al. FGF2-mediated reciprocal tumor cell-endothelial cell interplay contributes to the growth of chemoresistant cells: a potential mechanism for superficial bladder cancer recurrence [J]. | TUMOR BIOLOGY , 2016 , 37 (4) : 4313-4321 .
MLA Chen, Yule et al. "FGF2-mediated reciprocal tumor cell-endothelial cell interplay contributes to the growth of chemoresistant cells: a potential mechanism for superficial bladder cancer recurrence" . | TUMOR BIOLOGY 37 . 4 (2016) : 4313-4321 .
APA Chen, Yule , Zhu, Guodong , Wu, Kaijie , Gao, Yang , Zeng, Jin , Shi, Qi et al. FGF2-mediated reciprocal tumor cell-endothelial cell interplay contributes to the growth of chemoresistant cells: a potential mechanism for superficial bladder cancer recurrence . | TUMOR BIOLOGY , 2016 , 37 (4) , 4313-4321 .
Export to NoteExpress RIS BibTex
Infiltrating macrophages increase RCC epithelial mesenchymal transition (EMT) and stem cell-like populations via AKT and mTOR signaling SCIE PubMed Scopus
期刊论文 | 2016 , 7 (28) , 44478-44491 | ONCOTARGET | IF: 5.168
WoS CC Cited Count: 19 SCOPUS Cited Count: 19
Abstract&Keyword Cite

Abstract :

Infiltrating macrophages are a key component of inflammation during tumorigenesis and progression. However, the role of macrophages in renal cell carcinoma (RCC), especially in the stage of RCC malignant progression, is still unclear. Here, we found the macrophages could be recruited more easily into RCC tissues than the surrounding non-tumor tissues. In vitro co-culture system also confirmed RCC cells had a better capacity to recruit macrophages via CXCL8 signaling than normal renal epithelial cells. The consequences of recruiting more macrophages may then increase RCC cells invasion abilities. Mechanism dissection revealed that infiltrating macrophages could function through induction of epithelial-mesenchymal transition and increased cancer stem cell-like populations via activation of AKT/mTOR signal, and then led to increasing RCC cells invasion. The orthotopically xenografted mouse model with RCC cells and macrophages also confirmed that infiltrating macrophages could increase RCC cells progression via AKT/mTOR signal. Together, our results reveal a new mechanism that macrophages in the RCC tumor microenvironment could increase RCC metastasis via activation of the AKT/mTOR signals. Targeting this newly identified signaling may help us to better inhibit RCC metastasis.

Keyword :

AKT EMT macrophage stem cell RCC

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 Yang, Zhao , Xie, Hongjun , He, Dalin et al. Infiltrating macrophages increase RCC epithelial mesenchymal transition (EMT) and stem cell-like populations via AKT and mTOR signaling [J]. | ONCOTARGET , 2016 , 7 (28) : 44478-44491 .
MLA Yang, Zhao et al. "Infiltrating macrophages increase RCC epithelial mesenchymal transition (EMT) and stem cell-like populations via AKT and mTOR signaling" . | ONCOTARGET 7 . 28 (2016) : 44478-44491 .
APA Yang, Zhao , Xie, Hongjun , He, Dalin , Li, Lei . Infiltrating macrophages increase RCC epithelial mesenchymal transition (EMT) and stem cell-like populations via AKT and mTOR signaling . | ONCOTARGET , 2016 , 7 (28) , 44478-44491 .
Export to NoteExpress RIS BibTex
Interleukin-6 Drives Multiple Myeloma Progression By up-Regulating of CD147/Emmprin Expression CPCI-S SCIE
会议论文 | 2016 , 128 (22) | 58th Annual Meeting and Exposition of the American-Society-of-Hematology (ASH) | IF: 13.164
Abstract&Keyword Cite

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 Hu, Jinsong , Lei, Li , Wang, Yanmeng et al. Interleukin-6 Drives Multiple Myeloma Progression By up-Regulating of CD147/Emmprin Expression [C] . 2016 .
MLA Hu, Jinsong et al. "Interleukin-6 Drives Multiple Myeloma Progression By up-Regulating of CD147/Emmprin Expression" . (2016) .
APA Hu, Jinsong , Lei, Li , Wang, Yanmeng , Wang, Ke , Hu, Xiaoyan , Wang, Aiying et al. Interleukin-6 Drives Multiple Myeloma Progression By up-Regulating of CD147/Emmprin Expression . (2016) .
Export to NoteExpress RIS BibTex
YAP调控肾癌细胞迁移的机制研究
期刊论文 | 2016 , (11) | 现代泌尿外科杂志
Abstract&Keyword Cite

Keyword :

F-actin YAP 迁移能力 肾癌细胞

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 吕伟 , 徐珊 , 杨政 et al. YAP调控肾癌细胞迁移的机制研究 [J]. | 现代泌尿外科杂志 , 2016 , (11) .
MLA 吕伟 et al. "YAP调控肾癌细胞迁移的机制研究" . | 现代泌尿外科杂志 11 (2016) .
APA 吕伟 , 徐珊 , 杨政 , 范义增 , 李磊 , 吴开杰 et al. YAP调控肾癌细胞迁移的机制研究 . | 现代泌尿外科杂志 , 2016 , (11) .
Export to NoteExpress RIS BibTex
10| 20| 50 per page
< Page ,Total 3 >

Export

Results:

Selected

to

Format:
FAQ| About| Online/Total:3020/54984102
Address:XI'AN JIAOTONG UNIVERSITY LIBRARY(No.28, Xianning West Road, Xi'an, Shaanxi Post Code:710049) Contact Us:029-82667865
Copyright:XI'AN JIAOTONG UNIVERSITY LIBRARY Technical Support:Beijing Aegean Software Co., Ltd.