scholarly journals CircSERPINA3 regulates SERPINA3-mediated apoptosis, autophagy and aerobic glycolysis of prostate cancer cells by competitively binding to MiR-653-5p and recruiting BUD13

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Zengshu Xing ◽  
Sailian Li ◽  
Zhenxiang Liu ◽  
Chong Zhang ◽  
Zhiming Bai
Keyword(s):  
Prostate Cancer ◽  
Cell Apoptosis ◽  
Biological Function ◽  
Aerobic Glycolysis ◽  
Prostate Gland ◽  
Prostate Cancer Cells ◽  
Examine Gene Expression ◽  
Functional Analyses ◽  
The Relationship ◽  
Common Malignancy

Abstract Background Prostate cancer (PCa) belongs to an epithelial malignancy that occurs in the prostate gland and is the most common malignancy of the male genitourinary system. Referring to related literature, circSERPINA3 has been reported to be up-regulated in PCa. However, its biological function remains unclear. Purpose This study aimed to reveal the specific role and relevant molecular mechanism of circSERPINA3 in PCa. Methods RT-qPCR was used to examine gene expression and functional analyses were conducted to verify the effect of circSERPINA3 on cell apoptosis, autophagy and aerobic glycolysis in PCa cells. Mechanism assays were applied to evaluate the relationship among circSERPINA3/miR-653-5p/SERPINA3/BUD13. Results CircSERPINA3 was verified to be up-regulated in PCa cells and to inhibit cell apoptosis while promoting aerobic glycolysis and autophagy in PCa cells. CircSERPINA3 and SERPINA3 were also testified to bind to miR-653-5p through a line of mechanism experiments. Moreover, it was discovered that circSERPINA3 could stabilize SERPINA3 mRNA via recruiting BUD13. Additionally, SERPINA3 was verified to inhibit cell apoptosis, while promoting aerobic glycolysis and autophagy in PCa cells. Conclusions Our study suggested that circSERPINA3 regulated apoptosis, autophagy and aerobic glycolysis of PCa cells by competitively binding to miR-653-5p and recruiting BUD13. Graphic abstract

MiR-493 Induces Cytotoxic Autophagy in Prostate Cancer Cells through Regulation on PHLPP2

2020 ◽  
Vol 21 (14) ◽  
pp. 1451-1456 ◽  
Author(s):  
Jun Deng ◽  
Ming Ma ◽  
Wei Jiang ◽  
Liangliang Zheng ◽  
Suping Cui
Keyword(s):  
Prostate Cancer ◽  
Protein Expression ◽  
Cell Function ◽  
Mrna Levels ◽  
Prostate Cancer Cells ◽  
Potent Inducer ◽  
Qrt Pcr ◽  
Autophagy Gene ◽  
The Relationship ◽  
Cancer Inhibition

Background: MiR-493 promotes the proliferation of prostate cancer (PC) cells by targeting PHLPP2. We aimed to explore the relationship between miR-493 and autophagy in PC. Methods: qRT-PCR and western blotting were used to determine the mRNA levels and protein expression of miR-493, PHLPP2, autophagy gene BECN1 and ATG7 in PC cells. The autophagy gene expression was determined after PC cells transfected with miR-493 precursor or PHLPP2 precursor. Corresponding changes of autophagy phenotype and PC cell function were also studied. Results: The mRNA levels and protein expression of miR-493, PHLPP2, BECN1 and ATG7 in PC cells were significantly decreased in PC cells. Overexpression of miR-493 or PHLPP2 markedly upregulated the expression levels of BECN1 and ATG7 in PC cells. Overexpression of miR-493 and PHLPP2 markedly promoted autophagy, and inhibited the invasion and cloning formation of PC cells. Conclusion: MiR-493 is a potent inducer of cytotoxic autophagy that leads to prostate cancer inhibition by regulating on PHLPP2.

The Relationship of Prostate Gland Volume to Extended Needle Biopsy on Prostate Cancer Detection

2003 ◽  
Vol 169 (1) ◽  
pp. 130-135 ◽  
Author(s):  
JEAN O. UNG ◽  
IGNACIO F. SAN FRANCISCO ◽  
MEREDITH M. REGAN ◽  
WILLIAM C. DeWOLF ◽  
ARIA F. OLUMI
Keyword(s):  
Prostate Cancer ◽  
Cancer Detection ◽  
Needle Biopsy ◽  
Prostate Gland ◽  
Prostate Cancer Detection ◽  
Gland Volume ◽  
Relationship Of ◽  
The Relationship

scholarly journals Long noncoding RNA PCA3 regulates glycolysis, viability and apoptosis by mediating the miR-1/CDK4 axis in prostate cancer

RSC Advances ◽  
2018 ◽  
Vol 8 (66) ◽  
pp. 37564-37572 ◽  
Author(s):  
Shuo Gu ◽  
Xiaobing Niu ◽  
Fei Mao ◽  
Zongyuan Xu
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Aerobic Glycolysis ◽  
Prostate Cancer Cells

We proved that PCA3 regulated aerobic glycolysis, viability and apoptosis by regulating the miR-1/CDK4 axis in prostate cancer cells.

scholarly journals Inhibition of LOXL2 Enhances the Radiosensitivity of Castration-Resistant Prostate Cancer Cells Associated with the Reversal of the EMT Process

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Peng Xie ◽  
Hongliang Yu ◽  
Feijiang Wang ◽  
Feng Yan ◽  
Xia He
Keyword(s):  
Prostate Cancer ◽  
Cell Apoptosis ◽  
Castration Resistant Prostate Cancer ◽  
Prostate Cancer Cells ◽  
Castration Resistant ◽  
Du145 Cells ◽  
Androgen Independent

Introduction. Radiotherapy is the mainstay in the treatment of prostate cancer. However, significant radioresistance of castration-resistant prostate cancer (CRPC) cells constitutes a main obstacle in the treatment of this disease. By using bioinformatic data mining methods, LOXL2 was found to be upregulated in both androgen-independent prostate cancer cell lines and radioresistant tumor samples collected from patients with prostate cancer. We speculate that LOXL2 may play an important role in the radioresistance of CRPC cells. Methods. The effect of LOXL2 knockdown on the radiosensitivity of androgen-independent prostate cancer cells lines was measured by the clonogenic assay and xenograft tumor experiments under in vitro and in vivo conditions, respectively. In studies on the mechanism, we focused on the EMT phenotype changes and cell apoptosis changes induced by LOXL2 knockdown in DU145 cells. The protein levels of three EMT biomarkers, namely, E-cadherin, vimentin, and N-cadherin, were measured by western blotting and immunohistochemical staining. Cell apoptosis after irradiation was measured by flow cytometry and caspase-3 activity assay. Salvage experiment was also conducted to confirm the possible role of EMT in the radiosensitization effect of LOXL2 knockdown in CRPC cells. Results. LOXL2 knockdown in CRPC cells enhanced cellular radiosensitivity under both in vitro and in vivo conditions. A significant reversal of EMT was observed in LOXL2-silenced DU145 cells. Cell apoptosis after irradiation was significantly enhanced by LOXL2 knockdown in DU145 cells. Results from the salvage experiment confirmed the key role of EMT process reversal in the radiosensitization effect of LOXL2 knockdown in DU145 cells. Conclusions. LOXL2 plays an important role in the development of cellular radioresistance in CRPC cells. Targeting LOXL2 may be a rational avenue to overcome radioresistance in CRPC cells. A LOXL2-targeting strategy for CRPC treatment warrants detailed investigation in the future.

scholarly journals Statins induce cell apoptosis through a modulation of AKT/FOXO1 pathway in prostate cancer cells

2019 ◽  
Vol Volume 11 ◽  
pp. 7231-7242 ◽  
Author(s):  
Jun-Li Deng ◽  
Rui Zhang ◽  
Ying Zeng ◽  
Yuan-Shan Zhu ◽  
Guo Wang
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Cell Apoptosis ◽  
Prostate Cancer Cells ◽  
Induce Cell Apoptosis

Prostate epithelial cell differentiation and its relevance to the understanding of prostate cancer therapies

2004 ◽  
Vol 108 (1) ◽  
pp. 1-11 ◽  
Author(s):  
Ronan M. LONG ◽  
Colm MORRISSEY ◽  
John M. FITZPATRICK ◽  
R. William G. WATSON
Keyword(s):  
Prostate Cancer ◽  
Epithelial Cells ◽  
Prostate Gland ◽  
Western World ◽  
Cancer Therapies ◽  
Normal Prostate ◽  
Full Characterization ◽  
Prostate Epithelial Cells ◽  
Common Malignancy

Prostate cancer is the most common malignancy in males in the western world. However, little is known about its origin and development. This review highlights the biology of the normal prostate gland and the differentiation of basal epithelial cells to a secretory phenotype. Alterations in this differentiation process leading to cancer and androgen-independent disease are discussed, as well as a full characterization of prostate epithelial cells. A full understanding of the origin and characteristics of prostate cancer epithelial cells will be important if we are to develop therapeutic strategies to combat the heterogeneous nature of this disease.

794 MICRORNA-204 PROMOTES CELL APOPTOSIS BY TARGETING TO BCL-2 IN BLADDER AND PROSTATE CANCER CELLS

2013 ◽  
Vol 189 (4S) ◽  
Author(s):  
Thomas Hwang ◽  
Yi-Chia Lin ◽  
Te-Fu Tsai ◽  
Hung-En Chen ◽  
Kuang-Yu Chou ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Cell Apoptosis ◽  
Prostate Cancer Cells

Gambogic Acid Induces Cell Apoptosis and Inhibits MAPK Pathway in PTEN−/−/p53−/− Prostate Cancer Cells In Vitro and Ex Vivo

2017 ◽  
Vol 24 (2) ◽  
pp. 109-116 ◽  
Author(s):  
Hong Pan ◽  
Li-yuan Lu ◽  
Xue-qian Wang ◽  
Bin-xue Li ◽  
Kathleen Kelly ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Cell Apoptosis ◽  
Ex Vivo ◽  
Mapk Pathway ◽  
Gambogic Acid ◽  
Prostate Cancer Cells

KLF9, a transcription factor induced in flutamide-caused cell apoptosis, inhibits AKT activation and suppresses tumor growth of prostate cancer cells

The Prostate ◽  
2014 ◽  
Vol 74 (9) ◽  
pp. 946-958 ◽  
Author(s):  
Pengliang Shen ◽  
Jiabin Sun ◽  
Guiqin Xu ◽  
Li Zhang ◽  
Zhaojuan Yang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Transcription Factor ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Cell Apoptosis ◽  
Prostate Cancer Cells ◽  
Akt Activation

scholarly journals PKM2 Knockdown Induces Autophagic Cell Death via the AKT/mTOR Pathway in Human Prostate Cancer Cells

2019 ◽  
Author(s):  
Prasanta Dey ◽  
Amit Kundu ◽  
Richa Sachan ◽  
Jaehyun Park ◽  
Mee Young Ahn ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Cancer Metabolism ◽  
Aerobic Glycolysis ◽  
Autophagic Cell Death ◽  
Prostate Cancer Cells ◽  
Glucose Transporter 1 ◽  
Acridine Orange Staining ◽  
Cancer Tissues

Pyruvate kinase M2 (PKM2) is essential for aerobic glycolysis and is highly expressed in various cancer tissues. Although high PKM2 expression is observed in prostate cancer tissues, its functional role in cancer metabolism is unclear. Here, we investigated the role of PKM2 in regulating autophagy and its associated pathways in prostate cancer cells. PKM2 expression was silenced using various PKM2 small interfering RNAs (siRNAs) and then we measured PKM2-related cellular pathways associated with autophagy. PKM2 siRNA-transfected prostate cancer cells showed significantly reduced viability. Acridine orange staining and immunoblotting analysis showed that PKM2 downregulation markedly increased autophagic cell death. Results of western blotting analysis showed that PKM2 knockdown affected protein kinase B/mechanistic target of rapamycin 1 pathway, which consequently downregulated the expression of glycolytic enzymes lactate dehydrogenase A and glucose transporter 1. To the best of our knowledge, this is the first study to show that PKM2 inhibition alters cancer cell metabolism and induces autophagy. Thus, the present study provides a strategy for the development of PKM2-targeted novel anticancer drugs for the treatment of prostate cancer.

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