scholarly journals Ubenimex inhibits cell proliferation, migration and invasion by inhibiting the expression of APN and inducing autophagic cell death in prostate cancer cells

2016 ◽  
Vol 35 (4) ◽  
pp. 2121-2130 ◽  
Author(s):  
XIAOQING WANG ◽  
ZHIHONG NIU ◽  
YANG JIA ◽  
MENG CUI ◽  
LIPING HAN ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Cell Death ◽  
Cancer Cells ◽  
Autophagic Cell Death ◽  
Migration And Invasion ◽  
Prostate Cancer Cells

scholarly journals CAV3.1 knockdown suppresses cell proliferation, migration and invasion of prostate cancer cells by inhibiting AKT

2018 ◽  
Vol Volume 10 ◽  
pp. 4603-4614 ◽  
Author(s):  
Shanbiao Hu ◽  
Ling Li ◽  
Wei Huang ◽  
Jie Liu ◽  
Gongbin Lan ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Migration And Invasion ◽  
Prostate Cancer Cells

Pseudolaric Acid B Induces Caspase-Dependent Apoptosis and Autophagic Cell Death in Prostate Cancer Cells

2012 ◽  
Vol 27 (6) ◽  
pp. 885-891 ◽  
Author(s):  
Jing Tong ◽  
Shutao Yin ◽  
Yinhui Dong ◽  
Xiao Guo ◽  
Lihong Fan ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Autophagic Cell Death ◽  
Prostate Cancer Cells ◽  
Pseudolaric Acid B

Neuregulin promotes autophagic cell death of prostate cancer cells

The Prostate ◽  
2003 ◽  
Vol 55 (2) ◽  
pp. 147-157 ◽  
Author(s):  
Pazit Tal-Or ◽  
Ayelet Di-Segni ◽  
Zipora Lupowitz ◽  
Ronit Pinkas-Kramarski
Keyword(s):  
Prostate Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Autophagic Cell Death ◽  
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.

scholarly journals A Potential Antineoplastic Peptide of Human Prostate Cancer Cells Derived from the Lesser Spotted Dogfish (Scyliorhinus canicula L.)

Marine Drugs ◽  
2019 ◽  
Vol 17 (10) ◽  
pp. 585 ◽  
Author(s):  
Adrien Bosseboeuf ◽  
Amandine Baron ◽  
Elise Duval ◽  
Aude Gautier ◽  
Pascal Sourdaine ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Cell Death ◽  
Growth Inhibition ◽  
Cancer Cells ◽  
Apoptotic Cell ◽  
Prostate Cancer Cells ◽  
Cell Death Mechanisms ◽  
Autophagy Inhibition

The purpose of the present paper is to investigate the mechanism of action of a pyroglutamate-modified peptide (pE-K092D) on in vitro growth inhibition of MDA-Pca-2b prostate cancer cells. This peptide was derived from a peptide previously isolated from the testis of the lesser spotted dogfish and identified as QLTPEALADEEEMNALAAR (K092D). The effect of the peptide on cell proliferation and cell death mechanisms was studied by flow cytometry. Cellular morphology and cytoskeleton integrity of peptide-treated cells were observed by immunofluorescence microscopy. Results showed the onset of peptide induced early cytoskeleton perturbation, inhibition of autophagy, inhibition of cell proliferation and, at the end, non-apoptotic cell death mechanisms (membrane destabilization and necrosis). All those mechanisms seem to contribute to MDA-Pca-2b growth inhibition by a main cytostatic fate.

scholarly journals Resveratrol activates autophagic cell death in prostate cancer cells via downregulation of STIM1 and the mTOR pathway

2015 ◽  
Vol 55 (5) ◽  
pp. 818-831 ◽  
Author(s):  
Senthil Selvaraj ◽  
Yuyang Sun ◽  
Pramod Sukumaran ◽  
Brij B. Singh
Keyword(s):  
Prostate Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Mtor Pathway ◽  
Autophagic Cell Death ◽  
Prostate Cancer Cells

744 ZOLEDRONIC ACID INDUCES AUTOPHAGIC CELL DEATH IN HUMAN PROSTATE CANCER CELLS

2011 ◽  
Vol 185 (4S) ◽  
Author(s):  
Yi-Chia Lin ◽  
Ji-Fan Lin ◽  
Te-Fu Tsai ◽  
Kuang-Yu Chou ◽  
Hung-En Chen ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Death ◽  
Zoledronic Acid ◽  
Cancer Cells ◽  
Autophagic Cell Death ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells

scholarly journals Long non-coding RNA LINC01116 acts as an oncogene in prostate cancer cells through regulation of miR-744-5p/UBE2L3 axis

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Shengjie Yu ◽  
Huihong Yu ◽  
Yuanfeng Zhang ◽  
Chuan Liu ◽  
Weili Zhang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Migration And Invasion ◽  
Prostate Cancer Cells ◽  
Cancer Cell Growth ◽  
Non Coding Rna ◽  
The Relationship ◽  
Long Non Coding Rna

Abstract Background Long non-coding RNA (lncRNA) has been confirmed to exert a critical effect on the progression of tumors, including prostate cancer. Previous literature has demonstrated LINC01116 involves in activities of multiple cancers. However, the underlying role of LINC01116 in prostate cancer remains unclear. Methods qRT-PCR measured the expression of LINC01116 in prostate cancer cells. EdU experiment was used to detect cell proliferation. Transwell assays detected cell migration and invasion. Immunofluorescence staining and western blot assays were utilized to measure EMT progress. The binding relationship between RNAs was confirmed by a series of mechanism assays. In addition, rescue experiments were conducted to verify the relationship among RNAs. Results LINC01116 was found to be highly expressed in prostate cancer cells. Functional assays indicated that inhibition of LINC01116 could suppress cell proliferation, migration, invasion and EMT progress. Also, miR-744-5p was proven to bind with LINC01116. Moreover, UBE2L3 was verified as the target gene of miR-744-5p. In rescue assays, we discovered that inhibited miR-744-5p or overexpressed UBE2L3 could offset the suppressive influence of silencing LINC01116 on prostate cancer cells. Conclusion Our study suggested that lncRNA LINC01116 acted as an oncogene in prostate cancer and accelerated prostate cancer cell growth through regulating miR-744-5p/UBE2L3 axis.

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