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.

The function of long noncoding RNA HOTAIRM1 in the progression of prostate cancer cells

Andrologia ◽  
2020 ◽  
Author(s):  
Lei Wang ◽  
Longning Wang ◽  
Qingfen Wang ◽  
Bahman Yosefi ◽  
Sen Wei ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Prostate Cancer Cells

Knockdown of long noncoding RNA AC245100.4 inhibits the tumorigenesis of prostate cancer cells via the STAT3/NR4A3 axis

Epigenomics ◽  
2021 ◽  
Author(s):  
Chi Liu ◽  
Ping Lin ◽  
Jiabin Zhao ◽  
Hui Xie ◽  
Rou Li ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Rna Sequencing ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Transcriptional Repressor ◽  
Sequencing Analysis ◽  
Loss Of Function ◽  
Prostate Cancer Cells ◽  
Rna Immunoprecipitation

Aim: To explore the role and mechanism of long noncoding RNA AC245100.4 and NR4A3 in prostate cancer (PCa). Methods: RNA-sequencing analysis was used to detect the downstream genes of AC245100.4. A series of gain- and loss-of-function approaches were used to investigate the roles of AC245100.4 and NR4A3. RNA immunoprecipitation was performed to examine the interaction between AC245100.4 and STAT3. Results: AC245100.4 was significantly upregulated in PCa cells and tissues. Knockdown of AC21500.4 significantly inhibited the tumorigenesis of PCa cells. Mechanistically, AC245100.4 deregulated the transcription of NR4A3 via increasing p-STAT3, which acted as a transcriptional repressor of NR4A3. Conclusion: Knockdown of lncRNA AC245100.4 inhibits the tumorigenesis of PCa cells via the STAT3/ NR4A3 axis.

scholarly journals PCA3 long noncoding RNA modulates the expression of key cancer-related genes in LNCaP prostate cancer cells

Tumor Biology ◽  
2016 ◽  
Vol 37 (8) ◽  
pp. 11339-11348 ◽  
Author(s):  
Ana Emília Goulart Lemos ◽  
Luciana Bueno Ferreira ◽  
Nadia Maria Batoreu ◽  
Paula Priscilla de Freitas ◽  
Martin Hernan Bonamino ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Prostate Cancer Cells

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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