scholarly journals Bicalutamide enhances fodrin-mediated apoptosis through calpain in LNCaP

2018 ◽  
Vol 243 (10) ◽  
pp. 843-851 ◽  
Author(s):  
Jiyeong Lee ◽  
Sora Mun ◽  
Arum Park ◽  
Doojin Kim ◽  
Byung Heun Cha ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Western Blotting ◽  
Anticancer Drug ◽  
Test Group ◽  
Differentially Expressed ◽  
Potential Candidate ◽  
Differentially Expressed Proteins ◽  
Prostate Cancer Cells ◽  
Apoptosis Pathway

Prostate cancer is the most common cancer in men, and before it progresses and metastasizes, the anticancer drug bicalutamide is often administered to patients. Many cases of androgen-dependent prostate cancer develop resistance during treatment with bicalutamide. Therefore, the effect of bicalutamide on androgen-dependent LNCaP prostate cancer cells is of clinical interest. The aim of this study was to demonstrate the effects of the anticancer drug bicalutamide on LNCaP prostate cancer cells by using a proteomics approach. Based on the results, 314 proteins were differentially expressed between the LNCaP and LNCaP treated with bicalutamide. The apoptosis pathway associated with differentially expressed proteins was shown in the Kyoto Encyclopedia of Gene and Genome pathway mapper. The Kyoto Encyclopedia of Gene and Genome pathway mapper results revealed that the fodrin-mediated apoptosis pathway is associated with the actions of bicalutamide and Western blotting was performed to validate these results. Impact statement We studied bicalutamide’s anticancer action by using proteomics. The effect of bicalutamide on androgen-exposed LNCaP cells was also studied. KEGG identified >1.8-fold differentially expressed proteins between test group cells. KEGG mapper showed fodrin-mediated apoptosis involvement in bicalutamide’s action. The anticancer effects of bicalutamide, which was further confirmed using Western blotting. Therefore, this drug is a potential candidate for understanding bicalutamide’s effect on LNCaP and fodrin can be used as a biomarker monitoring status in metastatic carcinoma.

scholarly journals Citral Induced Apoptosis through Modulation of Key Genes Involved in Fatty Acid Biosynthesis in Human Prostate Cancer Cells: In Silico and In Vitro Study

2020 ◽  
Vol 2020 ◽  
pp. 1-15 ◽  
Author(s):  
Sri Renukadevi Balusamy ◽  
Haribalan Perumalsamy ◽  
Karpagam Veerappan ◽  
Md. Amdadul Huq ◽  
S. Rajeshkumar ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Fatty Acid ◽  
Cancer Cells ◽  
Fatty Acid Synthase ◽  
Human Prostate ◽  
Detection Methods ◽  
Potential Candidate ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells ◽  
Apoptosis Pathway

The isomers of citral (cis-citral and trans-citral) were isolated from the Cymbopogon citratus (DC.) Stapf oil demonstrates many therapeutic properties including anticancer properties. However, the effects of citral on suppressing human prostate cancer and its underlying molecular mechanism have yet to be elucidated. The citral was isolated from lemongrass oil using various spectroscopic analyses, such as electron ionized mass spectrometry (EI-MS) and nuclear magnetic resonance (NMR) spectroscopy respectively. We carried out 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay to evaluate the cell viability of citral in prostate cancer cells (PC-3 and PC3M). Furthermore, to confirm that PC3 undergoes apoptosis by inhibiting lipogenesis, we used several detection methods including flow cytometry, DNA fragmentation, Hoechst staining, PI staining, oil staining, qPCR, and Western blotting. Citral impaired the clonogenic property of the cancer cells and altered the morphology of cancer cells. Molecular interaction studies and the PASS biological program predicted that citral isomers tend to interact with proteins involved in lipogenesis and the apoptosis pathway. Furthermore, citral suppressed lipogenesis of prostate cancer cells through the activation of AMPK phosphorylation and downregulation of fatty acid synthase (FASN), acetyl coA carboxylase (ACC), 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGR), and sterol regulatory element-binding protein (SREBP1) and apoptosis of PC3 cells by upregulating BAX and downregulating Bcl-2 expression. In addition, in silico studies such as ADMET predicted that citral can be used as a safe potent drug for the treatment of prostate cancer. Our results indicate that citral may serve as a potential candidate against human prostate cancer and warrants in vivo studies.

scholarly journals Epigallocatechin gallate-zinc oxide co-crystalline nanoparticles as an anticancer drug that is non-toxic to normal cells

RSC Advances ◽  
2018 ◽  
Vol 8 (14) ◽  
pp. 7369-7376 ◽  
Author(s):  
Pawatsanai Samutprasert ◽  
Khajeelak Chiablaem ◽  
Chanon Teeraseranee ◽  
Punnawich Phaiyarin ◽  
Puttikorn Pukfukdee ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Zinc Oxide ◽  
Cancer Cells ◽  
Anticancer Drug ◽  
Zno Nanoparticles ◽  
Epigallocatechin Gallate ◽  
Prostate Cancer Cells ◽  
Tea Polyphenol ◽  
Normal Cells

A tea polyphenol, epigallocatechin-3-gallate (EGCG), can enhance cytotoxicity of Zinc in cancer cells. Here we synthesize hybrid EGCG-ZnO nanoparticles that can kill PC-3 prostate cancer cells at concentrations that are not toxic to normal cells.

Contribution of microRNA-200b-3p to radiation therapy resistance in 22RV1 prostate cancer cells.

2018 ◽  
Vol 36 (6_suppl) ◽  
pp. 89-89
Author(s):  
John Thoms ◽  
Satoko Aoki ◽  
Lourdes Pena Castillo
Keyword(s):  
Prostate Cancer ◽  
Radiation Therapy ◽  
Cancer Cells ◽  
Cell Lines ◽  
Clonogenic Survival ◽  
Negative Control ◽  
Differentially Expressed ◽  
Prostate Cancer Cells ◽  
Altered Expression ◽  
Resistant Phenotype

89 Background: Radiation therapy (RT) is a standard treatment option for men with localized prostate cancer. Despite having well-established treatment regimens, such men still fail RT at a rate of up to 30-50%. RT resistant phenotype is a key component leading to treatment failure. MicroRNAs (miRNAs) can influence the response to RT, and the abundance or lack of certain miRNAs can induce a RT resistant phenotype through alteration of survival pathways. We show that altered expression of miR-200b-3p plays an important role in contributing to RT resistance. Methods: RT resistant subline from the parental 22RV1 prostate cancer cell line was generated by exposure to fractionated RT – 22RV1-RT. The global expression level of miRNAs and mRNA was determined, using the Affymetrix GeneChip®: miRNA 4.0 and Human Gene 2.0 ST Arrays. Parental and 22RV1-RT cells were transfected with miR-200b-3p mimics or negative control. The influence of miR-200b-3p on cellular proliferation, morphology, migration, clonogenic survival and response to RT was determined by standard assays. Results: MiR-200b-3p was the only miRNA that was statistically differentially expressed between the two cell lines. There were 39 differentially expressed genes. Of the 65 genes predicted to be regulated by miR-200b-3p as identified from miRTarBase, only Fibronectin 1 (FN1) was in common. FN1 was up-regulated in 22RV1- RT cells. MiR-200b-3p mimics; in comparison to negative control mimics, suppressed cell proliferation in both cell lines. Both cell lines with negative control mimics have fibroblastic-type morphology and display a stretched shape following RT. While, cells transfected with miR-200b-3p mimics demonstrated a round morphology and formed clusters following RT. Over-expression of miR-200b-3p mimics inhibited cell migration synergically with RT and demonstrated a lower degree of clonogenic survival following RT in 22RV1-RT cells compared to negative control mimics. Surprisingly, miR-200b-3p mimics reversed the observed RT resistance and the sensitivity to RT was to the same degree as the parental 22RV1 cells. Conclusions: Together, these data suggest that miR-200b-3p independently contributes to RT resistance in 22RV1 prostate cancer cells.

scholarly journals hPEBP4 Resists TRAIL-induced Apoptosis of Human Prostate Cancer Cells by Activating Akt and Deactivating ERK1/2 Pathways

2006 ◽  
Vol 282 (7) ◽  
pp. 4943-4950 ◽  
Author(s):  
Hongzhe Li ◽  
Xiaojian Wang ◽  
Nan Li ◽  
Jianming Qiu ◽  
Yuanyuan Zhang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Treatment ◽  
Cancer Cells ◽  
Potential Candidate ◽  
Lncap Cells ◽  
Prostate Cancer Cells ◽  
Efficient Treatment ◽  
Akt Activation ◽  
Du145 Cells ◽  
Induced Apoptosis

The treatment options available for prostate cancer are limited because of its resistance to therapeutic agents. Thus, a better understanding of the underlying mechanisms of the resistance of prostate cancer will facilitate the discovery of more efficient treatment protocols. Human phosphatidylethanolamine-binding protein 4 (hPEBP4) is recently identified by us as an anti-apoptotic molecule and a potential candidate target for breast cancer treatment. Here we found the expression levels of hPEBP4 were positively correlated with the severity of clinical prostate cancer. Furthermore, hPEBP4 was not expressed in TRAIL-sensitive DU145 prostate cancer cells, but was highly expressed in TRAIL-resistant LNCaP cells, which show highly activated Akt. Interestingly, hPEBP4 overexpression in TRAIL-sensitive DU145 cells promoted Akt activation but inhibited ERK1/2 activation. The hPEBP4-overexpressing DU145 cells became resistant to TRAIL-induced apoptosis consequently, which could be reversed by PI3K inhibitors. In contrast, silencing of hPEBP4 in TRAIL-resistant LNCaP cells inhibited Akt activation but increased ERK1/2 activation, resulting in their sensitivity to TRAIL-induced apoptosis that was restored by the MEK1 inhibitor. Therefore, hPEBP4 expression in prostate cancer can activate Akt and deactivate ERK1/2 signaling, leading to TRAIL resistance. We also demonstrated that hPEBP4-mediated resistance to TRAIL-induced apoptosis occurred downstream of caspase-8 and at the level of BID cleavage via the regulation of Akt and ERK pathways, and that hPEBP4-regulated ERK deactivation was upstream of Akt activation in prostate cancer cells. Considering that hPEBP4 confers cellular resistance to TRAIL-induced apoptosis and is abundantly expressed in poorly differentiated prostate cancer, silencing of hPEBP4 suggests a promising approach for prostate cancer treatment.

scholarly journals Metabolic Reprogramming and Predominance of Solute Carrier Genes during Acquired Enzalutamide Resistance in Prostate Cancer

Cells ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 2535
Author(s):  
Shiv Verma ◽  
Eswar Shankar ◽  
E. Ricky Chan ◽  
Sanjay Gupta
Keyword(s):  
Prostate Cancer ◽  
Drug Resistance ◽  
Cancer Cells ◽  
Standard Of Care ◽  
Resistant Cell ◽  
Metabolic Reprogramming ◽  
Differentially Expressed ◽  
Pcr Analysis ◽  
Prostate Cancer Cells ◽  
Solute Carrier

Androgen deprivation therapy (ADT) is standard-of-care for advanced-stage prostate cancer, and enzalutamide (Xtandi®, Astellas, Northbrook, IL, USA), a second generation antiandrogen, is prescribed in this clinical setting. The response to this medication is usually temporary with the rapid emergence of drug resistance. A better understanding of gene expression changes associated with enzalutamide resistance will facilitate circumventing this problem. We compared the transcriptomic profile of paired enzalutamide-sensitive and resistant LNCaP and C4-2B prostate cancer cells for identification of genes involved in drug resistance by performing an unbiased bioinformatics analysis and further validation. Next-Gen sequencing detected 9409 and 7757 genes differentially expressed in LNCaP and C4-2B cells, compared to their parental counterparts. A subset of differentially expressed genes were validated by qRT-PCR. Analysis by the i-pathway revealed membrane transporters including solute carrier proteins, ATP-binding cassette transporters, and drug metabolizing enzymes as the most prominent genes dysregulated in resistant cell lines. RNA-Seq data demonstrated predominance of solute carrier genes SLC12A5, SLC25A17, and SLC27A6 during metabolic reprogramming and development of drug resistance. Upregulation of these genes were associated with higher uptake of lactic/citric acid and lower glucose intake in resistant cells. Our data suggest the predominance of solute carrier genes during metabolic reprogramming of prostate cancer cells in an androgen-deprived environment, thus signifying them as potentially attractive therapeutic targets.

scholarly journals ANTICANCER DRUG-INDUCED APOPTOSIS AND CYTOTOXICITY IN PROSTATE CANCER CELLS ARE MODULATED BY ORGAN-SPECIFIC STROMAL CELL FACTORS

2001 ◽  
Vol 1 (S3) ◽  
pp. 59-59
Author(s):  
Bal L. Lokeshwar ◽  
Kamalaveni R. Prabhakar ◽  
Tie Yan Shang ◽  
Zafiria Mourelatos ◽  
De-Quan Li
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Anticancer Drug ◽  
Stromal Cell ◽  
Prostate Cancer Cells ◽  
Drug Induced ◽  
Organ Specific ◽  
Induced Apoptosis
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