CAMK2N1 inhibits prostate cancer progression through androgen receptor-dependent signaling

Wang, Tao; Guo, Shuren; Liu, Zhuo; Wu, Liang; Li, Mingchao; Yang, Jun; Chen, Ruibao; Liu, Xiaohui; Xu, Hua; Cai, Shaoxin; Chen, Hui; Li, Weiyong; Xu, Shaohua; Wang, Liang; Hu, Zhiquan; Zhuang, Qianyuan; Wang, Liping; Wu, Kongming; Liu, Jihong; Ye, Zhangqun; Ji, Jun-Yuan; Wang, Chenguang; Chen, Ke

doi:10.18632/oncotarget.2511

Cited by 54 publications

(57 citation statements)

References 33 publications

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“…For example, antiangiogenic genes included septin 9 (SEPT9) and protein tyrosine phosphatase, nonreceptor type 23 (PTPN23), which inhibit EC proliferation and migration, respectively (28,30). The antitumorigenic genes included ADAMTS9, which blocks tumor growth by inhibition of Akt activation (25); DYRK1A, which inhibits the growth of AML cells (26), and CAMK2N1, which inhibits prostate cancer progression through androgen receptor-dependent signaling (27). These activities were in line with the originating tumors, suggesting that TECs derived from CRC with a Th1-TME express a set of "memory genes."…”

Section: Discussionmentioning

confidence: 99%

Matricellular protein SPARCL1 regulates tumor microenvironment–dependent endothelial cell heterogeneity in colorectal carcinoma

Naschberger¹,

Liebl²,

Schellerer³

et al. 2016

Journal of Clinical Investigation

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Section: Discussionmentioning

confidence: 99%

Matricellular protein SPARCL1 regulates tumor microenvironment–dependent endothelial cell heterogeneity in colorectal carcinoma

Naschberger¹,

Liebl²,

Schellerer³

et al. 2016

Journal of Clinical Investigation

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“…Immunohistochemical analysis of human breast cancer and tumor xenograft tissue was carried out as described 55,56 Tumor xenograft in nude mice MCF-7-control, MCF-7-lenti-let-7a, MCF-7-KRas, MCF-7-let-7a-KRas cells (2£10 6 cells per site) were injected into the mammary fat pad of 6-week-old BALB/c femal nude mice (Shanghai Slaccas). Long-release estradiol pellets (Innovative Research of America) were implanted the day before inoculation.…”

Section: Immunohistochemistry (Ihc) Stainingmentioning

confidence: 99%

Let-7a regulates mammosphere formation capacity through Ras/NF-κB and Ras/MAPK/ERK pathway in breast cancer stem cells

Xu¹,

Sun²,

Qin

et al. 2015

Cell Cycle

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Keywords: breast cancer stem cells, KRas, let-7a, mammosphere formation capacity, MAPK/ERK, NF-kB Abbreviations: BCSCs, breast cancer stem cells; MFE, mammosphere-forming efficiency Breast cancer stem cells (BCSCs) have the greatest potential to maintain tumorigenesis in all subtypes of tumor cells and were regarded as the key drivers of tumor. Recent evidence has demonstrated that BCSCs contributed to a high degree of resistance to therapy. However, how BCSCs self renewal and tumorigenicity are maintained remains obscure. Herein, our study illustrated that overexpression of let-7a reduced cell proliferation and mammosphere formation ability of breast cancer stem cells(BCSCs) in a KRas-dependent manner through different pathways in vitro and in vivo. To be specific, we provided the evidence that let-7a was decreased, and reversely the expression of KRas was increased with moderate expression in early stages (I/II) and high expression in advanced stages (III/IV) in breast cancer specimens. In addition, the negative correlation between let-7a and KRas was clearly observed. In vitro, we found that let-7a inhibited mammosphere-forming efficiency and the mammosphere-size via NF-kB and MAPK/ERK pathway, respectively. The inhibitory effect of let-7a on mammosphere formation efficiency and the size of mammospheres was abolished after the depletion of KRas. On the contrary, enforced expression of KRas rescued the effect of let-7a. In vivo, let-7a inhibited the growth of tumors, whereas the negative effect of let-7a was rescued after overexpressing KRas. Taken together, our findings suggested that let-7a played a tumor suppressive role in a KRas-dependent manner.

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“…Luciferase activity was normalized for transfection efficiency using b-galactosidase reporter as an internal control. The fold effect of expression vector was determined in comparison with the value of the empty expression vector cassette and statistical analyses were performed using the t test (22,26).…”

Section: Luciferase Assaysmentioning

confidence: 99%

“…Tumor weight was measured when mice were sacrificed on day 32 after cell implantation. Immunohistochemical staining under the standard procedure was conducted as previously described (2,22).…”

Section: In Vivo Tumor Implantationmentioning

confidence: 99%

Flightless I Homolog Represses Prostate Cancer Progression through Targeting Androgen Receptor Signaling

Wang

Song

Chen

et al. 2016

Clinical Cancer Research

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Purpose: Flightless I (FLII), member of the gelsolin superfamily of actin-remodeling proteins, functions as a transcriptional coregulator. We aim to evaluate a tumor-suppressive function of FLII in regulating androgen receptor (AR) in prostate cancer progression.Experimental Design: We examined FLII protein and mRNA expression in clinical prostate cancer specimens by immunohistochemistry. Kaplan-Meier analysis was conducted to evaluate the difference in disease-overall survival associated with the expression levels of FLII and AR. Prostate cancer cells stably expressing FLII or shRNA knockdown were used for functional analyses. Immunoprecipitation, Luciferase reporter, and immunofluorescence staining assays were performed to examine the functional interaction between FLII and AR.Results: Our analysis of the expression levels of FLII in a clinical gene expression array dataset showed that the expression of FLII was positively correlated with the overall survival of prostate cancer patients exhibiting high levels of AR expression. Examination of protein and mRNA levels of FLII showed a significant decrease of FLII expression in human prostate cancers. AR and FLII formed a complex in a ligand-dependent manner through the ligand-binding domain (LBD) of AR. Subsequently, we observed a competitive binding to AR between FLII and the ligand. FLII inhibited AR transactivation and decreased AR nuclear localization. Furthermore, FLII contributed to castration-sensitive and castration-resistant prostate cancer cell growth through AR-dependent signaling, and reintroduction of FLII in prostate cancer cells sensitized the cells to bicalutamide and enzalutamide treatment.Conclusions: FLII plays a tumor-suppressive role and serves as a crucial determinant of resistance of prostate cancer to endocrine therapies.

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CAMK2N1 inhibits prostate cancer progression through androgen receptor-dependent signaling

Cited by 54 publications

References 33 publications

Matricellular protein SPARCL1 regulates tumor microenvironment–dependent endothelial cell heterogeneity in colorectal carcinoma

Matricellular protein SPARCL1 regulates tumor microenvironment–dependent endothelial cell heterogeneity in colorectal carcinoma

Let-7a regulates mammosphere formation capacity through Ras/NF-κB and Ras/MAPK/ERK pathway in breast cancer stem cells

Flightless I Homolog Represses Prostate Cancer Progression through Targeting Androgen Receptor Signaling

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