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Resveratrol-Loaded Phytomedicines for Management of Cancer
Published in Mahfoozur Rahman, Sarwar Beg, Mazin A. Zamzami, Hani Choudhry, Aftab Ahmad, Khalid S. Alharbi, Biomarkers as Targeted Herbal Drug Discovery, 2022
Shakir Saleem, Ruqaiyah Khan, Sandeep Arora
Many in vitro studies have examined the anti-proliferative and proapop-totic activity of resveratrol in human prostate cancer cells, and its mechanism of action. It was found that the growth of LNCaP cells (hormone-sensitive cells), DU-145 (androgen-independent) cells, and PC-3 (hormone-independent line possessing dysfunctional androgen receptors) cells were arrested in a concentration-dependent manner. Resveratrol also antagonized the formation of free radicals in macrophages and reduced the oxidative stress within premalignant cells, and it decreased the production of NO in PC-3 and DU-145 cells, reducing growth and metastasis of prostate cancer (Ratan et al., 2002).
Endocrine Therapies
Published in David E. Thurston, Ilona Pysz, Chemistry and Pharmacology of Anticancer Drugs, 2021
In preclinical studies it was shown that when LNCaP cells (a prostate cancer cell line engineered to express elevated levels of AR as found in patients with advanced prostate cancer) were treated with enzalutamide, the expression of androgen-dependent genes PSA and TMPRSS2 was down-regulated. Surprisingly, bicalutamide up-regulated expression of these genes in the same experiment. Furthermore, in the VCaP cell line which overexpresses AR, enzalutamide induced apoptosis, whereas bicalutamide did not. Other studies highlighted the subtle difference in pharmacology between these two agents.
Pharmacology of Disogenin and Related Compounds
Published in Amritpal Singh Saroya, Contemporary Phytomedicines, 2017
Dioscin (1, 2, and 4 pmol/L) could significantly inhibit the viability of LNCaP cells in a time- and concentration-dependent manner. Flow cytometry revealed that the apoptosis rate was increased after treatment of LNCaP cells with dioscin for 24 h, indicating that apoptosis was an important mechanism by which dioscin inhibited cancer (Chen et al. 2014).
Simultaneous administration of EZH2 and BET inhibitors inhibits proliferation and clonogenic ability of metastatic prostate cancer cells
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2023
Aide Negri, Marina Marozzi, Daniela Trisciuoglio, Dante Rotili, Antonello Mai, Federica Rizzi
For this purpose, we tested the efficacy of GSK126 and JQ1 simultaneous administration in DU145 and PC3 cells, which are perhaps the two most characterised and widely used androgen-independent and metastatic PC cell lines that mimic the most advanced stages of the disease35. LNCaP cells, originally isolated as androgen-dependent cells35, were also included in the first part of the experimental design. First, we tested the effects of the combination on cell viability, cell proliferation, and clonogenic ability of the selected cell lines. Then, we measured how GSK126 and JQ1, given as single agents or in combination, affect the expression of EZH2, BRD4, H3K27me3, c-myc, and NF-kB. Finally, we measured the effects of the combination on cell cycle progression and investigated the mechanisms of cell death, focussing our attention on caspases activation and apoptosis induction.
LRP11 activates β-catenin to induce PD-L1 expression in prostate cancer
Published in Journal of Drug Targeting, 2020
Sishun Gan, Jianqing Ye, Jian Li, Chuanyi Hu, Junkai Wang, Da Xu, Xiuwu Pan, Chuanmin Chu, Jian Chu, Jing Zhang, Jingcun Zheng, Xiangmin Zhang, Jidong Xu, He Zhang, Fajun Qu, Xingang Cui
The contribution of LRP family and immune check points to the pathogenesis of PRAD has been well established. However, the potential cross-talk between these two crucial pathways has not been explored so far. Here, we demonstrate this cross-talk by showing that LRP11 could activate β-Catenin to induce PD-L1 expression and immunosuppression. Although we show positive association between LRP11 expression and PD-L1 expression in our samples and TCGA PRAD dataset, we noticed that PD-L1 expression pattern is quite heterogeneous. It suggests that PD-L1 expression was under the regulation of various factors. Thus, understanding the regulation mechanism of PD-L1 expression is essential for the optimisation of PD-L1 based immunotherapy as only a subgroup of patients respond to the treatment. Another important point in our study is that the effects of LRP were reproducible and consistent in PC-3 and LNCaP cell lines. LNCaP cell expresses androgen receptor (AR) while PC3 cell does not express AR. Thus, they provide a great opportunity to address whether the effect of LRP is dependent on AR. Our results suggest that the effects of LRP are unlikely to be dependent on AR status. A novel finding in our study is that LRP11 antibody could block the LRP11/PD-L1 induced immunosuppression in in-vitro assays. However, the therapeutic potential of LRP11 antibody remains to be tested in future in-vivo studies.
Plasmatic exosomes from prostate cancer patients show increased carbonic anhydrase IX expression and activity and low pH
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2020
Mariantonia Logozzi, Davide Mizzoni, Clemente Capasso, Sonia Del Prete, Rossella Di Raimo, Mario Falchi, Daniela F. Angelini, Alessandro Sciarra, Martina Maggi, Claudiu T. Supuran, Stefano Fais
Human prostate carcinoma cell line (LNCaP) is derived from a metastatic site (left supraclavicular lymph node) of a 50-year-old Caucasian male (blood type B+) with confirmed diagnosis of metastatic prostate carcinoma (IstitutodeiTumori di Milano). Tumour cells were negative for Mycoplasma contamination as routinely tested by PCR (Venor®GeM, Minerva Biolabs, Germany). The cells were maintained in RPMI 1640 without sodium bicarbonate culture medium at pH 6.5 supplemented with antibiotics and 10% foetal calf serum (FCS) (Invitrogen, Milan, Italy), at 37 °C in humidified 5% CO2. The acid cell culture medium (pH 6.5) was obtained by the addition of 1 M HCl solution. The pH was measured with a pH 123 Microprocessor pH Metre (Hanna Instruments, Milan, Italy). LNCaP cells were slowly adjusted to pH 6.5 for a sufficient time starting from unbuffered conditions, allowing tumour cells to acidify the microenvironment themselves. After five days in unbuffered medium, measured pH of the culture was 6.5. Thus, we progressively conditioned the pH of the cultures starting from 7.4 until pH 6.5 in a time ranging from three to four weeks, allowing the cells to not be exposed to short-term pH stress17.