Gallic acid: a dietary polyphenol that exhibits anti-neoplastic activities by modulating multiple oncogenic targets

2021 ◽  
Vol 21 ◽  
Author(s):  
Hardeep Singh Tuli ◽  
Hiral Mistry ◽  
Ginpreet Kaur ◽  
Diwakar Aggarwal ◽  
Vivek Kumar Garg ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Gallic Acid ◽  
Chemotherapeutic Drugs ◽  
Polyphenolic Compound ◽  
Anti Cancer ◽  
Bioactive Phytochemicals ◽  
Cellular Pathways ◽  
Near Future ◽  
Intense Research

: Phytochemicals are being used for thousands of years to prevent dreadful malignancy. Side effects of existing allopathic treatment have also initiated intense research in the field of bioactive phytochemicals. Gallic acid, a natural polyphenolic compound, exists freely as well as in polymeric forms. The anti-cancer properties of gallic acid are indomitable by a variety of cellular pathways such as induction of programmed cell death, cell cycle apprehension, reticence of vasculature and tumor migration, and inflammation. Furthermore, gallic acid is found to show synergism with other existing chemotherapeutic drugs. Therefore, the antineoplastic role of gallic acid suggests its promising therapeutic candidature in the near future. The present review describes all these aspects of gallic acid at a single platform. In addition nanotechnology-mediated approaches are also discussed to enhance bioavailability and therapeutic efficacy.

scholarly journals Advances and challenges in cancer treatment and nutraceutical prevention: the possible role of dietary phenols in BRCA regulation

2021 ◽  
Author(s):  
Haroon Khan ◽  
Fabiana Labanca ◽  
Hammad Ullah ◽  
Yaseen Hussain ◽  
Nikolay T. Tzvetkov ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Natural Products ◽  
Cancer Treatment ◽  
Clinical Aspects ◽  
Anti Cancer ◽  
Brca 1 ◽  
Brca 2 ◽  
The Impact ◽  
Cancer Activity

AbstractOver the years, the attention towards the role of phytochemicals in dietary natural products in reducing the risk of developing cancer is rising. Cancer is the second primary cause of mortality worldwide. The current therapeutic options for cancer treatment are surgical excision, immunotherapy, chemotherapy, and radiotherapy. Unfortunately, in case of metastases or chemoresistance, the treatment options become very limited. Despite the advances in medical and pharmaceutical sciences, the impact of available treatments on survival is not satisfactory. Recently, natural products are a great deal of interest as potential anti-cancer agents. Among them, phenolic compounds have gained a great deal of interest, thanks to their anti-cancer activity. The present review focuses on the suppression of cancer by targeting BRCA gene expression using dietary polyphenols, as well as the clinical aspects of polyphenolic agents in cancer therapy. They regulate specific key processes involved in cancer progression and modulate the expression of oncogenic proteins, like p27, p21, and p53, which may lead to apoptosis, cell cycle arrest, inhibition of cell proliferation, and, consequently, cancer suppression. Thus, one of the mechanisms underlying the anti-cancer activity of phenolics involves the regulation of tumor suppressor genes. Among them, the BRCA genes, with the two forms (BRCA-1 and BRCA-2), play a pivotal role in cancer protection and prevention. BRCA germline mutations are associated with an increased risk of developing several types of cancers, including ovarian, breast, and prostate cancers. BRCA genes also play a key role in the sensitivity and response of cancer cells to specific pharmacological treatments. As the importance of BRCA-1 and BRCA-2 in reducing cancer invasiveness, repairing DNA damages, oncosoppression, and cell cycle checkpoint, their regulation by natural molecules has been examined.

scholarly journals Role of cell cycle events and apoptosis in mediating the anti-cancer activity of a silver(I) complex of 4-hydroxy-3-nitro-coumarin-bis(phenanthroline) in human malignant cancer cells

2009 ◽  
Vol 602 (2-3) ◽  
pp. 203-214 ◽  
Author(s):  
Bhumika Thati ◽  
Andy Noble ◽  
Bernadette S. Creaven ◽  
Maureen Walsh ◽  
Malachy McCann ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cancer Cells ◽  
Anti Cancer ◽  
Cancer Activity

scholarly journals Gallic Acid Induces S and G2 Phase Arrest and Apoptosis in Human Ovarian Cancer Cells In Vitro

2021 ◽  
Vol 11 (9) ◽  
pp. 3807
Author(s):  
Zhiping He ◽  
Xingquan Liu ◽  
Fenghua Wu ◽  
Shaozhen Wu ◽  
Gary O’Neal Rankin ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Ovarian Cancer ◽  
Gallic Acid ◽  
Cell Lines ◽  
Ovarian Cancer Cells ◽  
The Us ◽  
Ic50 Values ◽  
G2 Phase

Ovarian cancer (OC) is among the top gynecologic cancers in the US with a death tally of 13,940 in the past year alone. Gallic acid (GA) is a natural compound with pharmacological benefits. In this research, the role of GA on cell proliferation, cell apoptosis, cell cycle-related protein expression was explored in OC cell lines OVCAR-3 and A2780/CP70. After 24, 48 and 72 h of GA treatment, the IC50 values in OVCAR-3 cells were 22.14 ± 0.45, 20.36 ± 0.18, 15.13 ± 0.53 μM, respectively and in A2780/CP70 cells IC50 values were 33.53 ± 2.64, 27.18 ± 0.22, 22.81 ± 0.56, respectively. Hoechst 33,342 DNA staining and flow cytometry results showed 20 μM GA exposure could significantly accelerate apoptosis in both OC cell lines and the total apoptotic rate increased from 5.34%(control) to 21.42% in OVCAR-3 cells and from 8.01%(control) to 17.69% in A2780/CP70 cells. Western blot analysis revealed that GA stimulated programmed OC cell death via a p53-dependent intrinsic signaling. In addition, GA arrested cell cycle at the S or G2 phase via p53-p21-Cdc2-cyclin B pathway in the same cells. In conclusion, we provide some evidence of the efficacy of GA in ovarian cancer prevention and therapy.

scholarly journals Role of DNA Damage and MMP Loss in Radiosensitization-Induced Apoptosis by Ellagic Acid in HeLa Cells

2020 ◽  
Vol 25775790 ◽  
pp. 1-1
Author(s):  
Vidhula R Ahire ◽  
◽  
Amit Kumar ◽  
Sushma Bhosle ◽  
Kaushala Prasad Mishra ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Cell Survival ◽  
Hela Cells ◽  
Ellagic Acid ◽  
Mitochondrial Membrane ◽  
Radiation Treatment ◽  
Γ Radiation ◽  
Anti Cancer

Ellagic acid (EA) is a polyphenol found in grapes, pomegranates, walnuts, etc. exhibits anti-cancer properties. The current study was conducted to understand the radiosensitizing role of EA on HeLa cells. Monotherapy of EA and radiation was initially studied on HeLa cells. The addition of EA before the radiation treatment subsequently made DNA more susceptible to damage thereby developing DNA beaks, which are known to be lethal for cell survival. This was evaluated by performing comet and γ-foci formation assay. Other assays which included cell-cycle distribution, clonogenic cell survival assay, mitochondrial membrane drop, and apoptosis were performed to evaluate the effect of EA with radiation. Our results demonstrate that, when cells were exposed to the combinatorial treatment of EA (10µM) and 2Gy of γ-radiation there was augmented cell death, lesser cell-proliferation, reduction in the colony-forming ability, increased DNA tail length, more number of γ-foci persisting even after 24h, enhanced apoptosis, augmented drop in the mitochondrial membrane potential and a G1 cell-cycle arrest. These results suggest that EA exhibits not only anti-cancer properties in terms of cell-death but also exhibits a radiosensitizing effect when given in combination with γ-radiation. Thus, it can be concluded that EA not only exhibits anticancer effects but also has potential in radiosensitizing HeLa cells.

scholarly journals The Role of miRNA-7 in the Biology of Cancer and Modulation of Drug Resistance

2021 ◽  
Vol 14 (2) ◽  
pp. 149
Author(s):  
Ewa Gajda ◽  
Małgorzata Grzanka ◽  
Marlena Godlewska ◽  
Damian Gawel
Keyword(s):  
Gene Expression ◽  
Drug Resistance ◽  
Multidrug Resistance ◽  
Cancer Progression ◽  
Cancer Therapies ◽  
Pathological Conditions ◽  
Non Coding Rna ◽  
Anti Cancer ◽  
Cellular Pathways

MicroRNAs (miRNAs, miRs) are small non-coding RNA (ncRNA) molecules capable of regulating post-transcriptional gene expression. Imbalances in the miRNA network have been associated with the development of many pathological conditions and diseases, including cancer. Recently, miRNAs have also been linked to the phenomenon of multidrug resistance (MDR). MiR-7 is one of the extensively studied miRNAs and its role in cancer progression and MDR modulation has been highlighted. MiR-7 is engaged in multiple cellular pathways and acts as a tumor suppressor in the majority of human neoplasia. Its depletion limits the effectiveness of anti-cancer therapies, while its restoration sensitizes cells to the administered drugs. Therefore, miR-7 might be considered as a potential adjuvant agent, which can increase the efficiency of standard chemotherapeutics.

scholarly journals Knockdown of PTOV1 and PIN1 Exhibit Common Phenotypic Anti-Cancer Effects in MDA-MB-231 Cells

2019 ◽  
Author(s):  
Shibendra Kumar Lal Karna ◽  
Faiz Ahmad ◽  
Bilal Ahmad Lone ◽  
Yuba Raj Pokharel
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Translational Regulation ◽  
Cancer Cell Proliferation ◽  
Nuclear Condensation ◽  
Similar Expression Profile ◽  
Anti Cancer ◽  
Hoechst Staining ◽  
Mcf 7

AbstractBackgroundEarlier, we have identified PTOV1 as a novel interactome of PIN1 in PC-3 cells. This study aims to explore the functional similarity and the common role of both genes in breast cancer cell proliferation.MethodsCTG, crystal violet assay, clonogenic assay, wound healing assay, cell cycle analysis, Hoechst staining and ROS measurement were performed to assess cell viability were performed after knocking down of PTOV1 and PIN1 by siRNAs in MDA-MB-231 and MCF-7 cells. CO-IP, qPCR and western blot were performed for interaction, transcriptional and translational regulation of both genes.ResultsKnockdown of PTOV1 and PIN1 inhibited the cell proliferation, colony formation, migration cell cycle, and induces nuclear condensation as well as ROS production. Interaction of PTOV1 and PIN1 was validated by Co-IP in MDA-MB-231 cells. Genes involved in cell proliferation, migration, cell cycle, and apoptosis were regulated by PIN1 and PTOV1. PTOV1 knockdown inhibited Bcl-2, Bcl-xL and induces BAX, LC3 and Beclin-1. Overexpression of PIN1 increased the expression of PTOV1. Knockdown of both genes inhibited the expression of cyclin D1, c-Myc, and β-catenin.ConclusionsPTOV1 and PIN1 interacts and exert oncogenic role in MDA-MB-231 cells by sharing the similar expression profile at transcriptional and translational level which can be a promising hub for therapeutic target.

Small Molecule CDK Inhibitors for the Therapeutic Management of Cancer

2020 ◽  
Vol 20 (17) ◽  
pp. 1535-1563 ◽  
Author(s):  
Bharat Goel ◽  
Nancy Tripathi ◽  
Nivedita Bhardwaj ◽  
Shreyans K. Jain
Keyword(s):  
Cell Cycle ◽  
Regulatory Subunit ◽  
Cdk Inhibitors ◽  
Primary Role ◽  
Regulatory Subunits ◽  
Protein Substrates ◽  
Anti Cancer ◽  
Multifunctional Enzymes ◽  
Inhibitor Genes

: Cyclin-dependent kinases (CDKs) are a group of multifunctional enzymes consisting of catalytic and regulatory subunits. The regulatory subunit, cyclin, remains dissociated under normal circumstances, and complexation of cyclin with the catalytic subunit of CDK leads to its activation for phosphorylation of protein substrates. The primary role of CDKs is in the regulation of the cell cycle. Retinoblastoma protein (Rb) is one of the widely investigated tumor suppressor protein substrates of CDK, which prevents cells from entering into cell-cycle under normal conditions. Phosphorylation of Rb by CDKs causes its inactivation and ultimately allows cells to enter a new cell cycle. Many cancers are associated with hyperactivation of CDKs as a result of mutation of the CDK genes or CDK inhibitor genes. Therefore, CDK modulators are of great interest to explore as novel therapeutic agents against cancer and led to the discovery of several CDK inhibitors to clinics. This review focuses on the current progress and development of anti-cancer CDK inhibitors from preclinical to clinical and synthetic to natural small molecules.

DNA methylation in satellite repeats disorders

2019 ◽  
Vol 63 (6) ◽  
pp. 757-771 ◽  
Author(s):  
Claire Francastel ◽  
Frédérique Magdinier
Keyword(s):  
Dna Methylation ◽  
Human Genome ◽  
Repetitive Dna ◽  
Dna Sequences ◽  
Satellite Repeats ◽  
Tremendous Progress ◽  
Genes Encoding ◽  
Dna Elements ◽  
Near Future

Abstract Despite the tremendous progress made in recent years in assembling the human genome, tandemly repeated DNA elements remain poorly characterized. These sequences account for the vast majority of methylated sites in the human genome and their methylated state is necessary for this repetitive DNA to function properly and to maintain genome integrity. Furthermore, recent advances highlight the emerging role of these sequences in regulating the functions of the human genome and its variability during evolution, among individuals, or in disease susceptibility. In addition, a number of inherited rare diseases are directly linked to the alteration of some of these repetitive DNA sequences, either through changes in the organization or size of the tandem repeat arrays or through mutations in genes encoding chromatin modifiers involved in the epigenetic regulation of these elements. Although largely overlooked so far in the functional annotation of the human genome, satellite elements play key roles in its architectural and topological organization. This includes functions as boundary elements delimitating functional domains or assembly of repressive nuclear compartments, with local or distal impact on gene expression. Thus, the consideration of satellite repeats organization and their associated epigenetic landmarks, including DNA methylation (DNAme), will become unavoidable in the near future to fully decipher human phenotypes and associated diseases.

Overview of Biological Therapy in Ulcerative Colitis: Current and Future Directions

2015 ◽  
Vol 24 (2) ◽  
pp. 203-213 ◽  
Author(s):  
Federica Furfaro ◽  
Cristina Bezzio ◽  
Sandro Ardizzone ◽  
Alessandro Massari ◽  
Roberto De Franchis ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Immunosuppressive Agents ◽  
Mucosal Healing ◽  
Aminosalicylic Acid ◽  
Proinflammatory Mediators ◽  
Experimental Drugs ◽  
New Treatments ◽  
Aggressive Clinical Course ◽  
Near Future

The treatment of ulcerative colitis (UC) has changed over the last decade. It is extremely important to optimize the therapies which are available nowadays and commonly used in daily clinical practice, as well as to stimulate the search for more powerful drugs for the induction and maintenance of sustained and durable remission, thus preventing further complications. Therefore, it is mandatory to identify the patients' prognostic variables associated with an aggressive clinical course and to test the most potent therapies accordingly.To date, the conventional therapeutic approach based on corticosteroids, salicylates (sulfasalazine, 5-aminosalicylic acid) or immunosuppressive agents is commonly used as a first step to induce and to maintain remission. However, in recent years, knowledge of new pathogenetic mechanisms of ulcerative colitis have allowed us to find new therapeutic targets leading to the development of new treatments that directly target proinflammatory mediators, such as TNF-alpha, cytokines, membrane migration agents, cellular therapies.The aim of this review is to provide the most significant data regarding the therapeutic role of drugs in UC and to give an overview of biological and experimental drugs that will become available in the near future. In particular, we will analyse the role of these drugs in the treatment of acute flare and maintenance of UC, as well as its importance in mucosal healing and in treating patients at a high risk of relapse.

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