scholarly journals Heterometallic titanium–gold complexes inhibit renal cancer cells in vitro and in vivo

2015 ◽  
Vol 6 (9) ◽  
pp. 5269-5283 ◽  
Author(s):  
Jacob Fernández-Gallardo ◽  
Benelita T. Elie ◽  
Tanmoy Sadhukha ◽  
Swayam Prabha ◽  
Mercedes Sanaú ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Renal Cancer ◽  
Anticancer Agents ◽  
Gold Complexes ◽  
First Time

Heterometallic compounds as anticancer agents demonstratingin vivopotential for the first time. Titanocene–gold derivatives: promising candidates for renal cancer.

scholarly journals Antitumor Potential of Marine and Freshwater Lectins

Marine Drugs ◽  
2019 ◽  
Vol 18 (1) ◽  
pp. 11 ◽  
Author(s):  
Elena Catanzaro ◽  
Cinzia Calcabrini ◽  
Anupam Bishayee ◽  
Carmela Fimognari
Keyword(s):  
Cancer Cells ◽  
Anticancer Agents ◽  
Complete Healing ◽  
Anticancer Compounds ◽  
Freshwater Organisms ◽  
Regulated Cell Death ◽  
Antitumor Potential ◽  
Unique Source

Often, even the most effective antineoplastic drugs currently used in clinic do not efficiently allow complete healing due to the related toxicity. The reason for the toxicity lies in the lack of selectivity for cancer cells of the vast majority of anticancer agents. Thus, the need for new potent anticancer compounds characterized by a better toxicological profile is compelling. Lectins belong to a particular class of non-immunogenic glycoproteins and have the characteristics to selectively bind specific sugar sequences on the surface of cells. This property is exploited to exclusively bind cancer cells and exert antitumor activity through the induction of different forms of regulated cell death and the inhibition of cancer cell proliferation. Thanks to the extraordinary biodiversity, marine environments represent a unique source of active natural compounds with anticancer potential. Several marine and freshwater organisms, ranging from the simplest alga to the most complex vertebrate, are amazingly enriched in these proteins. Remarkably, all studies gathered in this review show the impressive anticancer effect of each studied marine lectin combined with irrelevant toxicity in vitro and in vivo and pave the way to design clinical trials to assess the real antineoplastic potential of these promising proteins. It provides a concise and precise description of the experimental results, their interpretation as well as the experimental conclusions that can be drawn.

MP73-10 RITONAVIR, A POTENT INHIBITOR OF CYP3A4, ENHANCES THE ANTICANCER EFFECTS OF ENTINOSTAT IN RENAL CANCER CELLS IN VITRO AND IN VIVO

2017 ◽  
Vol 197 (4S) ◽  
Author(s):  
Takako Asano ◽  
Akinori Sato ◽  
Kazuki Okubo ◽  
Makoto Isono ◽  
Tomohiko Asano
Keyword(s):  
Cancer Cells ◽  
Renal Cancer ◽  
Potent Inhibitor ◽  
Anticancer Effects

scholarly journals Hyperbaric Oxygen Enhanced Mitochondria-Targeted Chemotherapy in Bladder Cancer

2020 ◽  
Author(s):  
Chongxing Shen ◽  
Xiaofeng Yue ◽  
Linyong Dai ◽  
Jianwu Wang ◽  
Jinjin Li ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Hyperbaric Oxygen ◽  
Cell Uptake ◽  
Bladder Cancer Cells ◽  
First Time ◽  
Mitochondria Targeting

Abstract Background: Bladder cancer has a high rate of recurrence and drug resistance due to a lack of effective therapies. IR-780 iodide, a near-infrared (NIR) mitochondria-targeting fluorescent agent, has been demonstrated to achieve higher selectivity than other drugs in different tumor types. In the study, we aimed to investigate the anti-tumor effect of IR-780 combined with hyperbaric oxygen (HBO) on bladder cancer.Methods: Using in vitro cell line data, in vivo model data and clinical data, we tested the ability of IR-780 to selectively accumulate in bladder cancer. We also evaluated the anti-tumor effect of IR-780 combined or not with HBO both in vitro and in vivo, and explored the potential mechanism of its anti-tumor effect. Results: We revealed for the first time that IR-780 selectively accumulated in bladder cancer (bladder cancer cells, xenografts and bladder cancer samples from patients) and could induce cancer cell apoptosis by targeting the mitochondrial complex I protein NDUFS1. Further study displayed that the combination with HBO could significantly enhance the antitumor effect of IR-780 in vitro by promoting cancer cell uptake and inducing excessive mitochondrial reactive oxygen species (ROS) production, while suppressing tumor growth and recurrence in animal models without causing apparent toxicity. Moreover, this combination antitumor strategy was also demonstrated in drug-resistant bladder cancer cells (T24/DDP) and xenografts. Conclusions: These data identify for the first time a combination of IR-780 and HBO (IR-780+HBO), which exhibits mitochondria-targeting and therapeutic capabilities, as a novel treatment paradigm for bladder cancer.

scholarly journals Cancer Associated Fibroblasts Promote Renal Cancer Progression Through a TDO/Kyn/AhR Dependent Signaling Pathway

2021 ◽  
Vol 11 ◽  
Author(s):  
Li-bo Chen ◽  
Shun-ping Zhu ◽  
Tian-pei Liu ◽  
Heng Zhao ◽  
Ping-feng Chen ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Renal Cancer ◽  
Cancer Progression ◽  
Cancer Associated Fibroblasts ◽  
Aromatic Hydrocarbon Receptor ◽  
Cancer Migration ◽  
Tumor Tissues ◽  
Enhanced Secretion

Cancer associated fibroblasts (CAFs) play crucial roles in cancer development, however, the specific mechanisms of CAFs associated renal cancer progression remain poorly understood. Our study observed enriched CAFs in high degree malignant tumor tissues from renal cancer patients. These CAFs isolated from tumor tissues are prone to facilitate drugs resistance and promote tumor progression in vitro and in vivo. Mechanistically, CAFs up-regulated tryptophan 2, 3-dioxygenase (TDO) expression, resulting in enhanced secretion of kynurenine (Kyn). Kyn produced from CAFs could up-regulated the expression of aromatic hydrocarbon receptor (AhR), eventually resulting in the AKT and STAT3 signaling pathways activation. Inhibition of AKT signal prevented cancer cells proliferation, while inhibition of the STAT3 signal reverted drugs resistance and cancer migration induced by kynurenine. Application of AhR inhibitor DMF could efficiently suppress distant metastasis of renal cancer cells, and improve anticancer effects of sorafenib (Sor)/sunitinib (Sun), which described a promising therapeutic strategy for clinical renal cancer.

Cell cycle arrest and senescence in P53-wild type renal carcinoma by enhancer RNA - P53-bound enhancer regions 2(p53BER2) through p53-dependent pathway

2020 ◽  
Author(s):  
HAIBIAO XIE ◽  
Kaifang Ma ◽  
Kenan Zhang ◽  
Jingcheng Zhou ◽  
Lei Li ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cancer Cells ◽  
Cell Lines ◽  
Kidney Cancer ◽  
Renal Cancer ◽  
G1 Arrest ◽  
Wild Type ◽  
Enhancer Rna

Abstract Background P53 is a classic tumor suppressor, but its role in kidney cancer remains unclear. In our study, we tried to explain the role of p53 in kidney cancer through p53 enhancer RNA-related pathway. Methods qPCR and luciferase reporters were used to detect the expression of p53-related enhancer RNA. Nutlin3 and artificial "microRNA" were used to induce and inhibit the expression of p53 enhancer RNA, respectively. Cycle analysis and β-galactosidase assay were used to explore whether P53-bound enhancer regions 2(p53BER2) plays a role in the cell cycle and senescence response of p53-wild type (WT) renal cancer cells. The function of p53BER2 was further analyzed in vivo by nude mice. RNA sequencing was used to identify the potential target of p53BER2. Results The results showed that P53BER2 expression was down-regulated in renal cancer tissues and cell lines and could specifically express in p53-WT renal cancer cell lines. Knockdown p53BER2 could reverse nutlin-3-induced cytotoxic effect in p53-WT cell lines. Further, downregulation of p53BER2 could reverse nutlin-3-induced G1 arrest and senescence in p53-WT cell lines. What is more, knockdown of p53BER2 showed a resistance to nutlin-3 treatment in Vivo. Additionally, we found BRCA2 could be regulated by p53BER2 in vitro and vivo, which suggested BRCA2 might mediate the function of p53BER2 in RCC. Conclusions The p53-associated enhancer RNA-p53BER2 mediates the cell cycle and senescence of p53 in p53-WT renal cancer cells. This further provides a novel approach and insight for the RCC and p53 research in renal cancer.

Exosome-mediated miR-9-5p promotes proliferation and migration of renal cancer cells both in vitro and in vivo by targeting SOCS4

2020 ◽  
Vol 529 (4) ◽  
pp. 1216-1224
Author(s):  
Wenbin Song ◽  
Yule Chen ◽  
Guodong Zhu ◽  
Hongjun Xie ◽  
Zhishang Yang ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Renal Cancer ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals An Aqueous Extract of Marine Microalgae Exhibits Antimetastatic Activity through Preferential Killing of Suspended Cancer Cells and Anticolony Forming Activity

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Syam Prakash Somasekharan ◽  
Amal El-Naggar ◽  
Poul H. Sorensen ◽  
Yuzhuo Wang ◽  
Hongwei Cheng
Keyword(s):  
Cancer Cells ◽  
Aqueous Extract ◽  
Anticancer Agents ◽  
Anticancer Activities ◽  
Antimetastatic Effect ◽  
Pancreatic Cancers ◽  
Subrenal Capsule ◽  
Nonadherent Cells

Research on marine natural products as potential anticancer agents is still limited. In the present study, an aqueous extract of a Canadian marine microalgal preparation was assessed for anticancer activities using various assays and cell lines of human cancers, including lung, prostate, stomach, breast, and pancreatic cancers, as well as an osteosarcoma.In vitro, the microalgal extract exhibited marked anticolony forming activity. In addition, it was more toxic, as indicated by increased apoptosis, to nonadherent cells (grown in suspension) than to adherent cells.In vivo, an antimetastatic effect of the extract was observed in NOD-SCID mice carrying subrenal capsule xenografts of PC3 prostate cancer cells. The results of the present study suggest that the antimetastatic effect of the aqueous microalgal extract is based on inhibition of colony forming ability of cancer cells and the preferential killing of suspended cancer cells. Further research aimed at identification of the molecular basis of the anticancer activities of the microalgal extract appears to be warranted.

scholarly journals Smart stimuli-responsive biofunctionalized niosomal nanocarriers for programmed release of bioactive compounds into cancer cells in vitro and in vivo

2021 ◽  
Vol 10 (1) ◽  
pp. 1895-1911
Author(s):  
Najmeh Alsadat Abtahi ◽  
Seyed Morteza Naghib ◽  
Fatemeh Haghiralsadat ◽  
Javad Zavar Reza ◽  
Fatemeh Hakimian ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Anticancer Agents ◽  
Tumor Model ◽  
Tween 80 ◽  
Chemotherapeutic Agents ◽  
Cancer Drug ◽  
Mouse Tumor ◽  
Transfection Efficacy

Abstract Cancer treatment is challenging due to late-stage diagnosis, drug resistance and systemic toxicity of chemotherapeutic agents. The formulation of the drug into nanoparticles (NPs) can enhance the treatment efficacy and effectiveness. Therefore, a new cationic niosomal formulation, which contains Tween 80, Tween 60, cholesterol and lysine amino acid as a platform model to enhance transfection efficacy and reach more acceptable stability, and curcumin (Cur) as a biological anti-cancer drug, are introduced. Here, the authors focused on the design and synthesis of novel lysine-mediated niosomal NPs for the effectual and controlled release of the antitumor agent, Cur, and turned to optimize niosome formulations, concerning the volume of cholesterol and surfactant to implement these anticancer agents, simultaneously. The characterization of NPs s was carried out and the results showed the successful synthesis of Cur-entrapped niosomal NPs with high efficacy, sufficient positive charges and a favorable size (95/33 nm). The in vitro studies have been performed to investigate the cytotoxicity, cellular uptake and apoptosis of normal and cancer cells treated by black niosome, free Cur and niosom-loaded Cur. The results showed that implementing agents by niosome caused enhanced cytotoxicity, uptake and anticancer activity in cancer cells in comparison with normal cells. Furthermore, the effect of this nanodrug was surveyed on the 4T1 xenografted Balb/C mouse tumor model. Cur delivery to cancer models caused a higher tumor inhibition rate than in other groups.

scholarly journals Tumor-Specific CTL Kill Murine Renal Cancer Cells Using Both Perforin and Fas Ligand-Mediated Lysis In Vitro, But Cause Tumor Regression In Vivo in the Absence of Perforin

2002 ◽  
Vol 168 (7) ◽  
pp. 3484-3492 ◽  
Author(s):  
Naoko Seki ◽  
Alan D. Brooks ◽  
Clive R. D. Carter ◽  
Timothy C. Back ◽  
Erin M. Parsoneault ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Renal Cancer ◽  
Fas Ligand ◽  
Tumor Regression
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