scholarly journals Review On the Effects Curcumin on Tumors of the Reproductive System

2021 ◽  
Vol 10 ◽  
pp. e2178
Author(s):  
Zahra Moradi ◽  
Yasaman Hekmatnia ◽  
Amin Dalili ◽  
Mostafa Sadeghi ◽  
Seyed Sina Neshat ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Cancer Cell ◽  
Reproductive System ◽  
Multiple Drug Resistance ◽  
Curcuma Longa ◽  
Cell Types ◽  
Multiple Drug ◽  
Protective Effects ◽  
Cancer Hallmarks ◽  
Anti Cancer

Curcumin, a polyphenolic derivative of Curcuma longa rhizome, has numerous beneficial effects, including antibacterial, anti-inflammatory, antiviral, antioxidant, antifungal, anti-ischemic, anti-cancer, hypoglycemic, nephroprotective, antirheumatic, hepato-protective, and antimutagenic. Curcumin has indicated the capability to exert anti-cancer activity by multifunctional mechanisms, such as induction of apoptosis, inhibition of cancer cell proliferation, cell cycle regulation, chemotherapeutic intestinal absorption, and modification of several cancer cell types signaling pathways. Several studies have shown that curcumin may have protective effects against tumors of the reproductive system. Reproductive system cancers may cause many undesirable physical and, especially, mental disorders. Infertility and its mental consequences, sexual problems, chemotherapy and surgery-related adverse effects, substantial economic burden, and death are the most common complications regarding the cancers of the reproductive system. By modulating several reproductive cancer hallmarks such as signaling pathways, multiple drug resistance, cancer cell growth and proliferation, tumor angiogenesis, and transcription factors, curcumin could be used as a safe, non-toxic, cheap, and easily accessible drug for treating different types of reproductive cancers. [GMJ.2021;10:e2178]

The antitoxic and protective effects of Curcuma longa and it`s active agent, Curcumin: оverview

2020 ◽  
pp. 66-72
Author(s):  
A. Khisamova ◽  
O. Gizinger
Keyword(s):  
Curcuma Longa ◽  
Physiological Activity ◽  
Active Agent ◽  
Modern Science ◽  
Physical Exertion ◽  
The Body ◽  
Modern World ◽  
Protective Effects ◽  
Daily Stress ◽  
Anti Cancer

In the modern world, where a person is exposed to daily stress, increased physical exertion, the toxic effect of various substances, including drugs. The task of modern science is to find antioxidants for the body. These can be additives obtained both synthetically and the active substances that we get daily from food. Such a striking example is turmeric, obtained from the plant Curcuma longa. Recently, it has been known that curcumin has an antioxidant, anti-inflammatory, anti-cancer effect and, thanks to these effects, plays an important role in the prevention and treatment of various diseases, in particular, from cancer to autoimmune, neurological, cardiovascular and diabetic diseases. In addition, much attention is paid to increasing the biological activity and physiological effects of curcumin on the body through the synthesis of curcumin analogues. This review discusses the chemical and physical characteristics, analogues, metabolites, the mechanisms of its physiological activity and the effect of curcumin on the body.

scholarly journals Vitamin E beyond Its Antioxidant Label

Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 634
Author(s):  
Anca Ungurianu ◽  
Anca Zanfirescu ◽  
Georgiana Nițulescu ◽  
Denisa Margină
Keyword(s):  
Vitamin E ◽  
Signaling Pathways ◽  
Molecular Mechanisms ◽  
Protective Effects ◽  
Cellular Effects ◽  
Inflammatory Status ◽  
Anti Cancer ◽  
Key Factor ◽  
Exciting Potential ◽  
Underlying Mechanisms

Vitamin E, comprising tocopherols and tocotrienols, is mainly known as an antioxidant. The aim of this review is to summarize the molecular mechanisms and signaling pathways linked to inflammation and malignancy modulated by its vitamers. Preclinical reports highlighted a myriad of cellular effects like modulating the synthesis of pro-inflammatory molecules and oxidative stress response, inhibiting the NF-κB pathway, regulating cell cycle, and apoptosis. Furthermore, animal-based models have shown that these molecules affect the activity of various enzymes and signaling pathways, such as MAPK, PI3K/Akt/mTOR, JAK/STAT, and NF-κB, acting as the underlying mechanisms of their reported anti-inflammatory, neuroprotective, and anti-cancer effects. In clinical settings, not all of these were proven, with reports varying considerably. Nonetheless, vitamin E was shown to improve redox and inflammatory status in healthy, diabetic, and metabolic syndrome subjects. The anti-cancer effects were inconsistent, with both pro- and anti-malignant being reported. Regarding its neuroprotective properties, several studies have shown protective effects suggesting vitamin E as a potential prevention and therapeutic (as adjuvant) tool. However, source and dosage greatly influence the observed effects, with bioavailability seemingly a key factor in obtaining the preferred outcome. We conclude that this group of molecules presents exciting potential for the prevention and treatment of diseases with an inflammatory, redox, or malignant component.

scholarly journals Verteporfin can Reverse the Paclitaxel Resistance Induced by YAP Over-Expression in HCT-8/T Cells without Photoactivation through Inhibiting YAP Expression

2016 ◽  
Vol 39 (2) ◽  
pp. 481-490 ◽  
Author(s):  
Wang Pan ◽  
Qian Wang ◽  
Yi Zhang ◽  
Naishu Zhang ◽  
Jiamin Qin ◽  
...  
Keyword(s):  
T Cells ◽  
Combination Therapy ◽  
Multiple Drug Resistance ◽  
Protein Detection ◽  
Multiple Drug ◽  
Over Expression ◽  
Anti Cancer ◽  
The Relationship ◽  
Proliferation And Invasion ◽  
Main Factor

Background/Aims: Paclitaxel (PTX) is one of the most effective anti-cancer drugs. However, multiple drug resistance is still the main factor that hinders the effective treatment of cancer with PTX. Several factors including YAP over-expression can cause PTX resistance. In this study, we aimed to verify the role YAP plays in PTX resistance, explore the reversal of PTX resistance by verteporfin (VP) and investigate the effect of combination therapy of PTX and VP on the PTX resistant colon cancer cells (HCT-8/T). Methods: To study the relationship between YAP and PTX resistance, a stable YAP-over-expression or YAP silencing cell line was generated by transfected with YAP-plasmids or siYAP-RNA. WST-1 assay was performed to detect the cytotoxicity of PTX on HCT-8 and HCT-8/T cells. Clone formation assay and Transwell assay was preformed to determine the cell proliferation and invasion ability respectively. Immunofluorescence and Western blot analysis was performed for protein detection. Results: YAP was stronger expressed in HCT-8/T than in HCT-8, and PTX resistance was positively correlated with the level of YAP expression. VP, a strongly YAP inhibitor, could reduce the PTX resistance on HCT-8/T cells without light activation by inhibiting YAP. Beside, VP and PTX combination therapy showed synergism on inhibition of YAP and cytotoxicity to HCT-8/T. Moreover, verteporfin and PTX combination therapy affect the invasion and colony formation ability and induce apoptosis of HCT-8/T cells. Conclusions: VP can reverse the PTX resistance induced by YAP over-expression in HCT-8/T cells without photoactivation through inhibiting YAP expression.

scholarly journals TTF1, in the Form of Nanoparticles, Inhibits Angiogenesis, Cell Migration and Cell Invasion in VitroandIn Vivoin Human Hepatoma through STAT3 Regulation

2016 ◽  
Author(s):  
Bin Xiao ◽  
Dongjing Lin ◽  
Xuan Zhang ◽  
Meilan Zhang ◽  
Xuewu Zhang
Keyword(s):  
Cell Migration ◽  
Cancer Cell ◽  
Hepg2 Cells ◽  
Binding Capacity ◽  
Hepatocellular Cancer ◽  
Cell Types ◽  
Tube Formation ◽  
Migration And Invasion ◽  
Nude Mouse Model ◽  
Anti Cancer

TTF1-NP(5,2′,4′-trihydroxy-6,7,5′-trimethoxyflavone nanoparticles), derived from the traditional Changbai Mountain medicinal plant Sorbaria sorbifolia (SS), has been showedits anti-cancer effect in various liver cancer cell types and tissues. The present study was designed to evaluate the antitumor mechanism of the TTF1-NP against HepG2 hepatoma cells and HepG2 cells-induced hepatocarcinoma (HCC) in nude mouse model. Here we demonstrated that TTF1-NP inhibits tube formation of HUVECs and HepG2 cell migration and invasion, and inhibits tumor growth in nude mice implanted with HepG2 cells through the downregulation of STAT3 protein and activation, along with VEGF, KDR, bFGF, MMP2 and MMP9 levels. We further revealed that TTF1-NP decreased the DNA-binding capacity of STAT3. Together our results provide a mechanism by which TTF1-NP suppresses cancer cell migration, invasion and angiogenesis through the action of STAT3 and suggests TTF1-NP as a potential therapy for hepatocellular cancer treatment.

scholarly journals 3,3′-Diindolylmethane Promotes Gastric Cancer Progression via β-TrCP-Mediated NF-κB Activation in Gastric Cancer-Derived MSCs

2021 ◽  
Vol 11 ◽  
Author(s):  
Hui Shi ◽  
Yaoxiang Sun ◽  
Hongru Ruan ◽  
Cheng Ji ◽  
Jiahui Zhang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Drug Resistance ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Multiple Drug Resistance ◽  
Cancer Drug ◽  
Multiple Drug ◽  
High Morbidity ◽  
Related Factors ◽  
Anti Cancer

Gastric cancer is a malignant tumor characterized by high morbidity and invasion. Surgery combined with chemo-radiotherapy is the most common treatment for gastric cancer, while multiple drug resistance always results in treatment failure. Once the anti-tumor drugs enter the tumor foci, tumor cells as well as those found in the microenvironment are affected. However, the effects of drugs on tumor microenvironment (TME) are easily overlooked. In this study, we investigated the effects of the anti-cancer drug 3,3’-diindolylmethane (DIM) on gastric cancer-derived mesenchymal stem cells (GC-MSCs) and their subsequent impact on cancer progression. Surprisingly, we found that the therapeutic concentration of DIM upregulated the expression level of tumor-related factors such as CCL-2, IL-6, and IL-8 in GC-MSCs. The conditioned medium of DIM-treated GC-MSCs promoted the proliferation, invasion, and migration of gastric cancer cells in vitro and tumor growth in vivo. Mechanistically, DIM enhanced the expression of β-TrCP, an E3 ubiquitin ligase leading to IκBα degradation and NF-κB activation in GC-MSCs. The β-TrCP knockdown partially eliminated positive results caused by DIM. Our results showed that the therapeutic dosage of DIM induced cell death in cancer cells, while enhancing MSC paracrine functions in the stroma to offset the original DIM effect on cancer cells. These findings provide a new mechanism of anti-cancer drug resistance and remind us to adjust the chemotherapeutic scheme by combining the anti-cancer drug with an appropriate signaling pathway inhibitor to block the side effects of drug on targeted TME cells.

scholarly journals Lanatoside C Induces G2/M Cell Cycle Arrest and Suppresses Cancer Cell Growth by Attenuating MAPK, Wnt, JAK-STAT, and PI3K/AKT/mTOR Signaling Pathways

Biomolecules ◽  
2019 ◽  
Vol 9 (12) ◽  
pp. 792 ◽  
Author(s):  
Dhanasekhar Reddy ◽  
Ranjith Kumavath ◽  
Preetam Ghosh ◽  
Debmalya Barh
Keyword(s):  
Cell Cycle ◽  
Cancer Cells ◽  
Signaling Pathways ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Mtor Signaling ◽  
Anti Cancer ◽  
Cancer Activity ◽  
Lanatoside C

Cardiac glycosides (CGs) are a diverse family of naturally derived compounds having a steroid and glycone moiety in their structures. CG molecules inhibit the α-subunit of ubiquitous transmembrane protein Na+/K+-ATPase and are clinically approved for the treatment of cardiovascular diseases. Recently, the CGs were found to exhibit selective cytotoxic effects against cancer cells, raising interest in their use as anti-cancer molecules. In this current study, we explored the underlying mechanism responsible for the anti-cancer activity of Lanatoside C against breast (MCF-7), lung (A549), and liver (HepG2) cancer cell lines. Using Real-time PCR, western blot, and immunofluorescence studies, we observed that (i) Lanatoside C inhibited cell proliferation and induced apoptosis in cell-specific and dose-dependent manner only in cancer cell lines; (ii) Lanatoside C exerts its anti-cancer activity by arresting the G2/M phase of cell cycle by blocking MAPK/Wnt/PAM signaling pathways; (iii) it induces apoptosis by inducing DNA damage and inhibiting PI3K/AKT/mTOR signaling pathways; and finally, (iv) molecular docking analysis shows significant evidence on the binding sites of Lanatoside C with various key signaling proteins ranging from cell survival to cell death. Our studies provide a novel molecular insight of anti-cancer activities of Lanatoside C in human cancer cells.

scholarly journals The natural product NI-07 demonstrates effective anti-cancer properties against numerous cancer cell types

2013 ◽  
Vol 3 (5) ◽  
Author(s):  
Lauren S. Gollahon ◽  
Kyungwoo Lee ◽  
Velvetlee Finckbone ◽  
Yunseong Jeong
Keyword(s):  
Natural Product ◽  
Cancer Cell ◽  
Cell Types ◽  
Anti Cancer

Role of the MDR-1-Encoded Multiple Drug Resistance Phenotype in Prostate Cancer Cell Lines

1993 ◽  
Vol 150 (5 Part 1) ◽  
pp. 1544-1547 ◽  
Author(s):  
Gerhard Theyer ◽  
Marion Schirmböck ◽  
Therese Thalhammer ◽  
Edward R. Sherwood ◽  
Gerhard Baumgartner ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Drug Resistance ◽  
Cell Lines ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Multiple Drug Resistance ◽  
Multiple Drug ◽  
Prostate Cancer Cell Lines ◽  
Mdr 1

The antiproliferative activity of ferrocene derivatives against drug-resistant cancer cell lines: A mini review

2021 ◽  
Vol 21 ◽  
Author(s):  
Li Li ◽  
Lin Ma ◽  
Jian Sun
Keyword(s):  
Drug Resistance ◽  
Cell Lines ◽  
Cancer Cell ◽  
Rational Design ◽  
Multiple Drug Resistance ◽  
Cancer Cell Lines ◽  
Multiple Drug ◽  
Drug Resistant ◽  
Ferrocene Derivatives ◽  
Preclinical Trial

: Cancer, a highly heterogeneous disease at intra/inter patient levels, remains a serious health problem contributing to significant morbidity and mortality worldwide. Despite great progress in clinical treatment, the concerns impeding the success of conventional cancer chemotherapy is descending efficacy of anticancer agents due to the development of drug resistance especially multiple drug resistance (MDR). Ferrocene derivatives have a different mode of action to the platinum anticancer drugs, and the ferrocene-phenol hybrid ferrocifen exhibits potential activity against drug-resistant cancers. Currently, ferrocifen is in preclinical trial, demonstrating that ferrocene derivatives are useful scaffolds for the development of novel anticancer candidates which are active against drug-resistant cancers. In the present review, the current scenario of ferrocene derivatives including ferrocene metal complexes, hybrids and other derivatives with antiproliferative potential against drug-resistant cancer cell lines is summarized for further rational design.

scholarly journals HIF1α inhibition by dual targeting of CDK4/6 and HSP90 reduces cancer cell viability including Rb-deficient cells

2020 ◽  
Author(s):  
Shuai Zhao ◽  
Lanlan Zhou ◽  
David T. Dicker ◽  
Avital Lev ◽  
Shengliang Zhang ◽  
...  
Keyword(s):  
Cell Viability ◽  
Cancer Cell ◽  
Hypoxia Inducible Factor ◽  
Heat Shock Protein 90 ◽  
Cell Types ◽  
Therapy Resistance ◽  
Hsp90 Inhibition ◽  
Multiple Cancer ◽  
Cancer Hallmarks

AbstractMost cancers harbor intra-tumoral hypoxia which promotes tumor progression and therapy resistance. Hypoxia-inducible factor 1α (HIF1α) mediates an adaptive response to hypoxia and contributes to multiple cancer hallmarks. We describe cancer therapeutic targeting of HIF1α by combination of CDK4/6 inhibitors (CDK4/6i) and heat-shock protein 90 inhibitors (HSP90i). CDK1 contributes to HSP90-mediated HIF1α stabilization whereas CDK1-knockdown enhances HIF1α reduction by HSP90i. Dual CDK1- and HSP90-inhibition increases apoptosis and synergistically inhibits cancer cell viability. To translate our findings, we use FDA-approved CDK4/6i in combination with HSP90i to reduce HIF1α expression and suppress viability of multiple cancer cell types, including Rb-deficient cancer cells. Overexpression of HIF1α668E partially rescues the cell viability inhibition by combination CDK4/6i and HSP90i treatment under hypoxia. CDK4/6i and HSP90i suppresses tumor growth in vivo. Thus, combined targeting of CDK4/6 and HSP90, through a drug class effect, inhibits HIF1α and shows preclinical anti-cancer therapeutic efficacy, including with Rb-deficiency.

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